CAP Quality Care / Seymann

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
Community‐acquired pneumonia: Defining quality care

The quality movement has spawned efforts to define and measure best practices for clinical conditions commonly cared for by hospitalists. Pneumonia is the most frequent infectious cause of death in the United States, and it accounts for more than 1 million hospitalizations annually at an estimated annual cost of $12.2 billion, most of it incurred by inpatients.1 The morbidity and mortality of the elderly are particularly burdensome.2, 3 For these reasons, attention has been focused on improving the quality of care of inpatients with community‐acquired pneumonia (CAP).

Credentialing agencies such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) require hospitals to report performance on predefined core measures of pneumonia care that they have identified as best practices (see Table 1).4, 5 The performance of individual organizations on these measures is now publicly reported at a website (www.hospitalcompare.hhs.gov) sponsored by the U.S. Department of Health and Human Services in conjunction with the Hospital Quality Alliance. Similar information is available at JCAHO's www.qualitycheck.org. Health care consumers can review quality data from the institution of their choice and compare the performance of various hospitals. The Centers for Medicare & Medicaid Services (CMS) provides financial incentives for the public reporting of such data and distributed $8.85 million to the top‐performing hospitals participating in a demonstration project in 2005.68 Voluntary reporting of performance on quality measures by individual physicians,9 as well as hospitals, is now being encouraged. As congress currently considers implementing pay for performance measures as a means to improve physician reimbursement, reporting will ultimately be linked to physician payments.

Core Measures of Quality Care for Pneumonia in Hospitalized Patients
  • Non‐ICU: B‐lactam + (macrolide or doxycycline) or respiratory fluoroquinolone.

  • ICU: B‐lactam + (macrolide or respiratory fluoroquinolone).

  • ICU with pseudomonal risk: IV antipseudomonal B‐lactam + (ciprofloxacin or levofloxacin) or antipseudomonal B‐lactam + aminoglycoside + ([ciprofloxacin or levofloxacin] or macrolide).

Collection of blood cultures before antibiotic therapy.
Collection of blood cultures within 24 hours of admission.
Mean time of less than 4 hours from arrival to initial administration of antibiotics.
Choice of initial antibiotics according to established guidelines.*
Pneumococcal screening and vaccination of eligible patients by discharge.
Influenza screening and vaccination of eligible patients during flu season.
Oxygenation assessment within 24 hours of admission.
Smoking cessation counseling to all smokers.

Performance on core measures for pneumonia is less consistent across hospitals than the other conditions currently being monitored.7 It is instructive, then, to review the evidence base for the existing pneumonia quality measures, which can inform decisions about prioritizing interventions to provide the most effective care for inpatients with CAP.

BLOOD CULTURES

In a large multicenter retrospective study of Medicare patients hospitalized with CAP, Meehan et al.10 found the performance of blood cultures within 24 hours of arrival to be associated with reduced 30‐day mortality. Despite the large sample size of more than 14,000 patients, the risk‐adjusted mortality reduction was of only borderline significance (RR 0.9 [0.81‐1.00]). The unadjusted data did not show a significant mortality reduction. Notably, collection of blood cultures prior to antibiotic administration did not affect mortality, even excluding patients receiving prehospital antibiotics.

A smaller review of 38 U.S. academic medical centers showed relatively high compliance with blood culture performance, but no mortality reduction, even after adjustment for severity of illness. Similarly, performing blood cultures before administration of antibiotics yielded no significant effect.11

Several studies call into question the clinical utility of performing blood cultures drawn from patients with CAP. Combined, these studies evaluated almost 3000 pneumonia patients who had blood cultures drawn; the likelihood of a change in therapy based on results was at most 5%. Among the patients with positive cultures, only 20%‐40% had a treatment change based on the result.1215

The more severely ill patients with CAP may benefit from blood cultures, though the findings reported in the literature vary.12, 16 Using the Pneumonia Severity Index (PSI) score17 to classify severity of illness, an observational study of 209 inpatients with CAP found the yield of blood cultures increased from 10% in the lowest‐risk groups to 27% in the most severely ill.16 In contrast, two larger studies with a combined enrollment of almost 14,000 patients were unable to demonstrate a difference in the incidence of bacteremia despite adjustment for the PSI score.12, 18 It is clear from these and other studies that patients in PSI classes I‐III derive very little benefit from the performance of blood cultures.12, 16, 19

Metersky et al.18 described a prospectively validated risk assessment tool that reliably predicted bacteremia in Medicare patients with CAP and explored its utility in reducing unnecessary blood cultures. Independent risk factors for bacteremia included prior antibiotic use, liver disease, hypotension, tachycardia, fever or hypothermia, BUN > 30 mg/dL, sodium < 130 mmol/L, and WBC < 5000 or > 20,000/mm2. Use of this tool predicted bacteremia in 89% of patients and avoided 39% of unnecessary blood cultures. The authors also tested a modified version of the tool that excluded the laboratory abnormalities, so rapid assessment could be made at the initial patient presentation. This version advocated a single blood culture for most patients, and 2 blood cultures for patients with 2 or more risk factors. The modified tool accurately identified 88% of the patients with bacteremia and enabled a 44% reduction in unnecessary cultures.

In summary, blood cultures occasionally provide useful clinical information about etiology and resistance patterns, but they do not seem to reliably influence therapeutic decisions. It seems inappropriate to recommend against their use in practice, but they are not a solid benchmark for evidence‐based quality care. Measures that mandate risk assessment of all inpatients with CAP and require blood cultures only for older patients or those judged at high risk by PSI may better reflect quality. Alternatively, performing blood cultures on patients deemed to be high risk by the model of Metersky et al.18 may suffice.

ANTIBIOTIC TIMING

In a study of Medicare patients by Meehan et al.,10 the 30‐day mortality rate was reduced by 15% in the subset of patients who received antibiotics within 8 hours of arrival at the hospital. However, a trend toward mortality reduction was noted for those receiving antibiotics as early as 6 hours after arrival. Rapid administration of antibiotics was thus deemed an important measure of the quality of care of patients with CAP.

Additional studies attempted to confirm this observation. Battleman et al.20 evaluated 700 patients admitted for CAP through the emergency department. They found that a delay of more than 8 hours in the administration of antibiotics was correlated with a prolonged inpatient stay. Mortality rates were not reported. Achieving rapid delivery of antibiotics was closely linked to administration of the first dose of antibiotics in the emergency department.

Conversely, a large retrospective review by Dedier et al.11 found no reduction in inpatient mortality or in length of stay based on rapid antibiotic delivery, despite adjustment for severity of illness. They did not evaluate 30‐day mortality.

The effect of antibiotic timing on the time to clinical stability has also been investigated. Clinical stability was defined as 24 hours of a systolic blood pressure 90 mm Hg, heart rate 100 beats/min, respiratory rate 24 breaths/min, temperature 38.3C (101F), room air oxygen saturation 90%, and the ability to eat. Silber et al.,21 in a review of the records of 409 inpatients with moderate to severe CAP by PSI score, compared patients receiving antibiotics less than 4 hours, between 4 and 8 hours, and more than 8 hours after hospital admission. There was no difference between groups in time to clinical stability, even with adjustment for PSI.

Marrie and Wu22 attempted to define the factors that influenced inpatient mortality of patients with CAP not admitted to the intensive care unit (ICU). In a prospective study of 3043 patients evaluating a clinical pathway, a multivariate analysis showed antibiotic administration within 4 hours was not correlated with reduced mortality.

Although most studies supporting rapid antibiotic delivery used a target of 8 hours, administration in less than 4 hours is the consensus standard for pneumonia care set by CMS and JCAHO.23, 24

A benefit of timing antibiotic administration less than 4 hours after admission has been confirmed by a single, very large retrospective study of Medicare patients at least 65 years old.25 Analysis of a random sample of more than 18,000 patients with CAP who had not received prehospital antibiotics showed that the relative risk reduction for inpatient mortality was 15% in the group receiving antibiotics within 4 hours. Thirty‐day mortality was similarly reduced, and benefits continued for every hour of early antibiotic administration up to 9 hours.

The absolute risk reduction was small, however (0.6%), yielding a number needed to treat of 167 patients to prevent 1 death.

Randomized controlled trials, which would more definitively address the issue of antibiotic timing, are unlikely, as intentionally delaying administration of antibiotics to patients with known CAP is unethical. Hence, reliance on observational data must suffice. Intuitively, it makes sense to begin treatment of a bacterial infection at the earliest time possible. However, it is also known that not all patients present in a typical fashion, and diagnosis is uncertain at least 20% of the time.26 Anecdotal reports suggest that incentivizing physicians on performance measures encourages premature administration of empiric antibiotics to all patients presenting with cough, prior to confirmation of pneumonia.27, 28 Such practices promote further antibiotic resistance, arguably a larger health issue than delay in antibiotic delivery.29, 30

Houck31 offers potential solutions to this problem, such as eliminating the pressure on hospitals to perform at 100% on this measure by reporting performance within acceptable ranges (eg, 70%‐84% and 85%‐100%) Targeting a benchmark of 80% or a duration of 6 hours may also be appropriate. Finally, a 4‐hour benchmark has not been shown to benefit younger patients, so it is important to apply this target only to patients more than 65 years of age.

CHOICE OF ANTIBIOTIC

A retrospective review of 12,945 cases of inpatients with CAP found that, in comparison to ceftriaxone alone, initial antibiotic regimens consisting either of a second‐ or third‐generation cephalosporin plus a macrolide or of a fluoroquinolone alone were associated with an approximately 30% reduction in 30‐day mortality.32 Hence, current guidelines recommend the combination of a B‐lactam and macrolide, a B‐lactam and doxycycline, or a respiratory fluoroquinolone for inpatients with CAP not admitted to the ICU.3335

The results of subsequent studies supported the contention that guideline‐compliant antibiotics improve outcomes. A prospective multicenter study of a clinical pathway that encouraged use of either levofloxacin or cefuroxime plus azithromycin for the initial treatment of inpatient CAP showed significantly reduced mortality. Compared with any other antibiotic regimen, the odds ratio for death was 0.22 with the cephalosporin/macrolide combination and 0.43 with the fluoroquinolone. Of note, early mortality (within 5 days of admission) was not reduced by antibiotic choice.22 Similar results were found in a retrospective analysis, which found the odds of 30‐day mortality increased by 5.7 in patients not receiving guideline‐compliant therapy.36 A third study found guideline‐compliant antibiotics reduced the likelihood of a prolonged length of stay by 45%.20

Of note, data on the effectiveness of the cephalosporin/doxycycline combination are limited, and the major guidelines differ about whether this regimen is appropriate for inpatients with CAP.33, 34 Important findings from a recent retrospective cohort study showed that initial therapy with ceftriaxone plus doxycycline was associated with reduced inpatient mortality (OR = 0.26) as well as reduced 30‐day mortality (OR = 0.37) compared with other guideline‐compliant therapies for CAP.37 When patients who would not have been considered appropriate for initial doxycycline therapy (those resident in nursing homes, with aspiration pneumonia, or in the ICU) were excluded, a large reduction in inpatient mortality remained (OR = 0.17), without any increase in length of stay or readmission rate. Interestingly, this study suggests the potential superiority of this regimen, though a randomized controlled trial is needed to confirm this. The current core measures do include doxycycline as an acceptable option for CAP therapy (see Table 1).

Currently, controversy remains about whether the benefit of these selected regimens results from their activity against atypical pathogens (Mycoplasma, Legionella, Chlamydia) and whether there is additional benefit from using combination antibiotic therapy.38, 39 Waterer40 described 225 inpatients with bacteremic pneumococcal pneumonia, noting the antibiotic regimen received during the first 24 hours of hospitalization. Patients were classified retrospectively into 3 groupssingle effective therapy (SET), dual effective therapy (DET), or more than dual effective therapy (MET)on the basis of the concordance of pneumococcal sensitivity with the initial antibiotics. Patients on 2 antibiotics were classified in the DET group if the organism was sensitive to both and in the SET group if the organism was resistant to 1 of the 2. Those in the MET group were analyzed separately, as they were found to have a higher baseline severity of illness based on the PSI score; the SET and DET groups were equivalent.

Surprisingly, the SET group was found to have a 3‐fold increase in inpatient mortality; adjustment for severity of illness increased the odds ratio for death to 6.4. Of note, all deaths were in the most severely ill patients (PSI IV‐V). The protective effects of receiving DET were not specifically limited to those receiving a macrolide as the second agent, and multivariate analysis did not find coverage of atypical organisms to be an independent predictor of mortality.

A recent prospective multicenter trial of 844 patients with bacteremic pneumococcal pneumonia at 21 hospitals confirmed these findings.41 A significant 14‐day survival advantage (23% versus 55%) was found in the subgroup of critically ill patients who received at least 2 effective antibiotics. Though survival benefit was restricted to the sickest patients, severity of illness was similar among the groups.

The specific importance of macrolides in combination therapy remains under investigation. A review of a database of inpatients with bacteremic pneumococcal pneumonia over a 10‐year period found that 58% received initial empiric therapy with a B‐lactam/macrolide combination and 42% received B‐lactam without a macrolide (though other antibiotic combinations were not excluded).42 After logistic regression analysis, the investigators found a relative reduction in inpatient mortality of 60% in the patients receiving combination therapy with macrolides. Unfortunately, neither comparison to fluoroquinolone monotherapy nor risk stratification by PSI was reported. A similar study from Canada that did stratify for risk confirmed a mortality benefit of combination therapy.43

A subsequent, extremely large study of more than 44,000 patients from a hospital claims‐made database lent support to these findings.44 This study included all CAP patients regardless of microbiology and was not restricted to those with bacteremia. Outcomes among groups receiving monotherapy with any of the standard agents for CAP were compared with those in groups receiving combination therapy with a macrolide as the second agent. Statistically significant reductions in 30‐day mortality were observed in all groups receiving dual therapy with macrolides. Consistent with other studies, the benefit applied only to patients with more severe CAP. The percentage of patients with bacteremia was not specified.

Of note, this study did not allow direct comparison of fluoroquinolone monotherapy to combination therapy with a B‐lactam and a macrolide. However, the fluoroquinolone/macrolide combination conferred no additional benefit beyond fluoroquinolone monotherapy when adjusted for severity of illness or age. This implies that fluoroquinolone monotherapy is adequate, at least in some subpopulations. This is consistent with initial studies that established the superiority of the antibiotic combinations recommended by the guidelines.20, 22, 32

The potential benefit of combination therapy appears limited to patients with higher severity of illness and pneumococcal bacteremia. However, outcomes are affected by the antibiotic regimen selected in the initial 24‐48 hours of hospitalization, before results of blood cultures are routinely available. At present, clinical prediction of patients who will benefit from combination therapy is difficult.

Coverage of undiagnosed mixed infections with atypical organisms is probably not a major factor benefiting patients receiving combination therapy. Several recent meta‐analyses found no reduction in mortality or the rate of clinical failure among patients receiving antibiotics covering atypical organisms compared with those for patients whose regimens did not have such coverage.4547 Subgroups of patients with Legionella pneumonia do benefit from antibiotics with targeted activity against atypical organisms, but fewer than 1% of all patients were so identified. Evidence for antibiotic synergy is similarly lacking.48, 49 The immunomodulatory effects of macrolides, which decrease cytokine production and inflammation and subsequently reduce the severity of lung injury and other complications of sepsis, are considered potential factors in the reduction of mortality.50

The definition of severe CAP and the indications for ICU admission remain controversial, evidence for which is reviewed elsewhere.34, 51, 52 Antibiotic recommendations for ICU patients are included in Table 1 for completeness, but a detailed review of the evidence is lacking because current guidelines are based on consensus opinion.34 The use of fluoroquinolone monotherapy in severe CAP is not currently recommended because of limitations of the existing evidence. The majority of quinolone trials have excluded severely ill patients, and approval trials of newer respiratory fluoroquinolones have used levofloxacin as a comparator. Studies comparing fluoroquinolones typically allowed investigators in the B‐lactam arm the option of adding macrolides or tetracycline at their discretion. In addition, such trials have been designed as noniferiority trials.38 Clearly, randomized controlled trials are needed to resolve this issue.

Currently, selecting appropriate antibiotics should follow established guidelines, with consideration of using combination therapy for patients with a higher severity of illness. Emphasis on this measure should be stronger than that on antibiotic timing, as the bulk of the evidence favors significant mortality reduction from following guidelines for antibiotic therapy.

VACCINATION

Guidelines recommend all eligible adults hospitalized with CAP receive pneumococcal vaccination on discharge,3335, 53 though there is no evidence this reduces the incidence of pneumonia or death.54, 55 Retrospective studies have shown reduced incidence of invasive disease (bacteremia and meningitis), but not of other end points.5457 The estimated mortality from pneumococcal bacteremia remain as high as 20%‐30%, with no evidence that this rate has decreased over the last 30 years.5861 Despite this, a recent meta‐analysis from the Cochrane database that included only randomized, controlled trials (75,197 patients in 15 trials) was unable to show significant reductions in all‐cause pneumonia or mortality for vaccinated subjects.62 Cohort studies, evaluated separately in this analysis, showed an efficacy of 53% in reducing the incidence of invasive pneumococcal disease. Given the relatively low incidence of invasive disease in the general population, the number needed to treat was estimated at 20,000, or 4000 if only older patients were considered. A subsequent retrospective cohort study showed no reduction in pneumonia hospitalizations, cases of outpatient pneumonia, or mortality among 45,365 elderly vaccinees.56 Some specific subgroups may benefit, however. Vaccinated patients with chronic lung disease did show a reduction in hospitalization for pneumonia (RR 0.57 [0.38‐0.84]) and in mortality (RR 0.7 [0.56‐0.9]) in a retrospective study of HMO patients older than age 65.63

It is of interest that since the licensure of the pediatric 7‐valent protein‐polysaccharide conjugate vaccine in 2000, the incidence of invasive pneumococcal disease among adults has dropped significantly. Overall reduction in invasive disease in adults more than 50 years old was 11% from 1998 to 2003 (relative risk reduction [RRR] = 28%). This is likely the result of decreased transmission from colonized or infected children and not a coincidental increase in adult pneumococcal vaccination, as the rates of disease caused by the 16 strains unique to the 23‐valent vaccine did not change.64, 65 The overall reduction in the incidence of invasive disease is still superior with the adult vaccine, up to 30% in vaccinated subjects (RRR = 44%).56 Invasive disease caused specifically by penicillin‐nonsusceptible serotypes has dropped by 49% in the elderly since introduction of the vaccine.66 Thus, the combined impact of the 2 vaccines may be significant. It is not yet clear what effect, if any, the 7‐valent vaccine will have on the hospitalization rate or mortality.

In contrast to the results for pneumococcal vaccination, studies of the benefits of influenza vaccination have shown clear and consistent reductions in mortality, respiratory illness, hospitalization, and pneumonia, especially among patients with comorbidities.6771 Cost effectiveness has been demonstrated for all populations,72, 73 and the reduction in mortality among high‐risk patients younger than age 65 has been estimated to be as high as 78%.68 Among the elderly, reduction in mortality of about 50% has been reported, along with 20%‐30% reductions in hospitalizations for pneumonia, influenza, cardiac disease, and stroke.70 Reduced incidence of pneumonia in vaccinated patients has even been documented among elderly patients without specific comorbidities.67 Annual revaccination has the most significant impact on mortality.74

The pneumococcal vaccine remains important in the effort to reduce the severity of and complications from invasive pneumococcal disease in the elderly, but the lack of significant benefits on hard end points such as mortality or hospitalizations makes it a less robust measure of quality pneumonia care. In contrast, influenza vaccination has a much larger impact on outcomes in the population at risk. Emphasis should be shifted from pneumococcal to influenza vaccine in pneumonia performance measures.

OXYGENATION ASSESSMENT

It seems intuitive that oxygenation assessment is important in the initial evaluation of patients with CAP, though there is not direct evidence to support this. The recommendation for oxygenation assessment in the published guidelines for CAP is by consensus.3335 Documented hypoxemia is associated with increased pneumonia‐related mortality,17, 75 and clinical judgment does not adequately predict hypoxemia.76 Though the assessment of oxygenation has been found to vary widely among practitioners,77 performance has remained consistent since the advent of monitoring and reporting of quality measures, with compliance rates of 99%.4, 7 Monitoring performance of this measure should continue, though high compliance rates limit its ability to discriminate among institutions.

SMOKING CESSATION COUNSELING

Counseling patients to stop smoking was found to be modestly (2%) but statistically significantly effective in promoting abstinence at 1 year.78 In its report on treating tobacco use, the U.S. Public Health Services recommended that all smokers receive hospital‐ and system‐based interventions at every visit.79 As part of the Pneumonia Patient Outcomes Research Team (PORT) study, smokers with pneumonia underwent a tobacco cessation interview. Though only 15% of these patients quit smoking, 93% of those who quit did so at the time they developed CAP.80 A retrospective study of patients with bacteremic pneumococcal pneumonia found tobacco exposure, including passive smoking, to be a strong independent risk factor for invasive disease.81 The most recent CAP guidelines from the Infectious Disease Society of America (IDSA) recommend smoking cessation counseling for all hospitalized patients who smoke.33 However, hospitals are not likely to have the impact that a more comprehensive, outpatient‐based smoking cessation program would. Without ongoing support, counseling, and pharmacotherapy, the effects of an intervention would be expected to be small.79 Though evidence of benefit is limited, smoking cessation interventions should be encouraged at all sites of care. Quality care merits this regardless of admitting diagnosis, but benefits specific to CAP outcomes have not yet been demonstrated.

CONCLUSIONS

The burden of illness caused by CAP mandates that clinicians strive to deliver the highest quality of care to afflicted patients. Critical evaluation of the strength of the evidence will continue to guide such endeavors, and changes in practice will follow as new information surfaces. Standards of care, as adopted by consensus groups such as the IDSA and American Thoracic Society, will continue to inform the practice of hospitalists.

How quality is defined for public reporting requires particularly careful assessment. The definition of quality should be based on evidence more rigorous than that ascribed to consensus guidelines. Within the profession, guidelines offer reasonable standards of care and delineate areas for further research and are invaluable tools for practicing clinicians. In the public arena, however, proclaiming practices as good or bad sets expectations of health care consumers not educated in the nuances of evaluating clinical evidence and can unfairly bias them against conscientious and effective providers whose standards reflect different interpretations of controversial issues. Regulatory agencies should publicly target interventions using only the most solid evidentiary foundation while internally striving to monitor the effects of different practice patterns and report measurable differences in outcomes revealed by careful investigation. Areas where controversy remains should be the primary targets of further research but should not be offered as benchmarks for public scrutiny until the medical community has settled on a position.

Furthermore, when evidence remains questionable, financial incentives should be linked to performance indicators with extreme caution. It would be counterproductive if health care organizations, driven to achieve optimal antibiotic timing to obtain payment updates from CMS, began to administer antibiotics prior to completing workups on all patients with respiratory complaints, as this would likely lead to antibiotic overuse. Similarly, institutions pushed to collect blood cultures before antibiotics are given may inappropriately delay administration in order to perform well on quality measures, resulting in potential harm to patients.

The measures of quality care for CAP for which the evidence on outcomes is the most convincing are antibiotic selection (mortality benefit, reduction in LOS) and influenza vaccination (mortality benefit, reduction in hospitalizations, reduction in respiratory illness). Antibiotic timing also shows a smaller but convincing reduction in mortality, though the advantages of receiving antibiotics within 4 hours instead of 8 hours are not clearly established for younger patients. These measures should be emphasized most heavily in the arena of public reporting and incentives for quality care, with additions and modifications guided by emerging evidence. Revision of the other measures to conform with current evidence would allow public reporting to more accurately reflect quality.

References
  1. Colice GL,Morley MA,Asche C,Birnbaum HG.Treatment costs of community‐acquired pneumonia in an employed population.Chest.2004;125:21402145.
  2. Kaplan V,Clermont G,Griffin MF, et al.Pneumonia: still the old man's friend?Arch Intern Med.2003;163:317323.
  3. Fry A SD,Holman R,Curns A,Anderson L.Trends in hospitalizations for pneumonia among persons aged 65 years or older in the United States, 1988‐2002.JAMA.2005;294:27122719.
  4. Williams SC,Schmaltz SP,Morton DJ,Koss RG,Loeb JM.Quality of care in U.S. hospitals as reflected by standardized measures, 2002‐2004.N Engl J Med.2005;353:255264.
  5. Performance Measurement: Core Measures. Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/index.htm. Accessed November 7, 2005.
  6. Medicare Quality Improvement Program Priorities: DRAFT, August2005.Centers for Medicare 353:265274.
  7. Medicare demonstration shows hospital quality of care improves with payments tied to quality.Centers for Medicare 278:20802084.
  8. Dedier J,Singer DE,Chang Y,Moore M,Atlas SJ.Processes of care, illness severity, and outcomes in the management of community‐acquired pneumonia at academic hospitals.Arch Intern Med.2001;161:20992104.
  9. Campbell SG,Marrie TJ,Anstey R,Dickinson G,Ackroyd‐Stolarz S.The contribution of blood cultures to the clinical management of adult patients admitted to the hospital with community‐acquired pneumonia: a prospective observational study.Chest.2003;123:11421150.
  10. Chalasani NP,Valdecanas MA,Gopal AK,McGowan JE,Jurado RL.Clinical utility of blood cultures in adult patients with community‐acquired pneumonia without defined underlying risks.Chest.1995;108:932936.
  11. Corbo J,Friedman B,Bijur P,Gallagher EJ.Limited usefulness of initial blood cultures in community acquired pneumonia.Emerg Med J.2004;21:446448.
  12. Waterer GW,Jennings SG,Wunderink RG.The impact of blood cultures on antibiotic therapy in pneumococcal pneumonia.Chest.1999;116:12781281.
  13. Waterer GW,Wunderink RG.The influence of the severity of community‐acquired pneumonia on the usefulness of blood cultures.Respir Med.2001;95(1):7882.
  14. Fine MJ,Auble TE,Yealy DM, et al.A prediction rule to identify low‐risk patients with community‐acquired pneumonia.N Engl J Med.1997;336:243250.
  15. Metersky ML,Ma A,Bratzler DW,Houck PM.Predicting bacteremia in patients with community‐acquired pneumonia.Am J Respir Crit Care Med.2004;169:342347.
  16. Theerthakarai R,El‐Halees W,Ismail M,Solis RA,Khan MA.Nonvalue of the initial microbiological studies in the management of nonsevere community‐acquired pneumonia.Chest.2001;119:181184.
  17. Battleman DS,Callahan M,Thaler HT.Rapid antibiotic delivery and appropriate antibiotic selection reduce length of hospital stay of patients with community‐acquired pneumonia: link between quality of care and resource utilization.Arch Intern Med.2002;162:682688.
  18. Silber SH,Garrett C,Singh R, et al.Early administration of antibiotics does not shorten time to clinical stability in patients with moderate‐to‐severe community‐acquired pneumonia.Chest.2003;124:17981804.
  19. Marrie TJ,Wu L.Factors influencing in‐hospital mortality in community‐acquired pneumonia: a prospective study of patients not initially admitted to the ICU.Chest.2005;127:12601270.
  20. Hospital Quality Measures:2004‐2007. Available at: http://www.cms.hhs.gov/quality/hospital/. Accessed November 17, 2005.
  21. National Hospital Quality Measures Specification Manual version 1.02.Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/aligned_manual.htm.
  22. Houck PM,Bratzler DW,Nsa W,Ma A,Bartlett JG.Timing of antibiotic administration and outcomes for Medicare patients hospitalized with community‐acquired pneumonia.Arch Intern Med.2004;164:637644.
  23. Metersky ML,Sweeney TA,Getzow MB,Siddiqui F,Nsa W,Bratzler DW.Antibiotic timing and diagnostic uncertainty in Medicare patients with pneumonia: is it reasonable to expect all patients to receive antibiotics within 4 hours?Chest.2006;130:1621.
  24. Houck PM,Bratzler DW.Administration of first hospital antibiotics for community‐acquired pneumonia: does timeliness affect outcomes?Curr Opin Infect Dis.2005;18(2):151156.
  25. Thompson D.The pneumonia controversy: hospitals grapple with 4 hour benchmark.Ann Emerg Med.2006;47:259261.
  26. Gonzales R,Bartlett JG,Besser RE, et al.Principles of appropriate antibiotic use for treatment of acute respiratory tract infections in adults: background, specific aims, and methods.Ann Intern Med.2001;134:479486.
  27. Garau J.The hidden impact of antibacterial resistance in respiratory tract infection. Clinical failures: the tip of the iceberg?Respir Med2001;95Suppl A:S511; discussion S26S27.
  28. Houck PM.Antibiotics and pneumonia: is timing everything or just a cause of more problems?Chest.2006;130:13.
  29. Gleason PP,Meehan TP,Fine JM,Galusha DH,Fine MJ.Associations between initial antimicrobial therapy and medical outcomes for hospitalized elderly patients with pneumonia.Arch Intern Med.1999;159:25622572.
  30. Mandell LA,Bartlett JG,Dowell SF,File TM,Musher DM,Whitney C.Update of practice guidelines for the management of community‐acquired pneumonia in immunocompetent adults.Clin Infect Dis.2003;37:14051433.
  31. Niederman MS,Mandell LA,Anzueto A, et al.Guidelines for the management of adults with community‐acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention.Am J Respir Crit Care Med.2001;163:17301754.
  32. Bartlett JG,Dowell SF,Mandell LA,File TM,Musher DM,Fine MJ.Practice guidelines for the management of community‐acquired pneumonia in adults.Infectious Diseases Society of America.Clin Infect Dis.2000;31:347382.
  33. Mortensen EM,Restrepo M,Anzueto A,Pugh J.Effects of guideline‐concordant antimicrobial therapy on mortality among patients with community‐acquired pneumonia.Am J Med.2004;117:726731.
  34. Flanders SA,Dudas V,Kerr K,McCulloch CE,Gonzales R.Effectiveness of ceftriaxone plus doxycycline in the treatment of patients hospitalized with community‐acquired pneumonia.J Hosp Med.2006;1:712.
  35. Waterer GW.Monotherapy versus combination antimicrobial therapy for pneumococcal pneumonia.Curr Opin Infect Dis.2005;18:157163.
  36. Weiss K,Tillotson GS.The controversy of combination vs monotherapy in the treatment of hospitalized community‐acquired pneumonia.Chest.2005;128:940946.
  37. Waterer GW,Somes GW,Wunderink RG.Monotherapy may be suboptimal for severe bacteremic pneumococcal pneumonia.Arch Intern Med.2001;161:18371842.
  38. Baddour LM,Yu VL,Klugman KP, et al.Combination antibiotic therapy lowers mortality among severely ill patients with pneumococcal bacteremia.Am J Respir Crit Care Med.2004;170:440444.
  39. Martinez JA,Horcajada JP,Almela M, et al.Addition of a macrolide to a beta‐lactam‐based empirical antibiotic regimen is associated with lower in‐hospital mortality for patients with bacteremic pneumococcal pneumonia.Clin Infect Dis.2003;36:389395.
  40. Weiss K,Low DE,Cortes L, et al.Clinical characteristics at initial presentation and impact of dual therapy on the outcome of bacteremic Streptococcus pneumoniae pneumonia in adults.Can Respir J.2004;11:589593.
  41. Brown RB,Iannini P,Gross P,Kunkel M.Impact of initial antibiotic choice on clinical outcomes in community‐acquired pneumonia: analysis of a hospital claims‐made database.Chest.2003;123:15031511.
  42. Shefet D,Robenshtok E,Paul M,Leibovici L.Empirical atypical coverage for inpatients with community‐acquired pneumonia: systematic review of randomized controlled trials.Arch Intern Med.2005;165:19922000.
  43. Shefet D,Robenshtock E,Paul M,Leibovici L.Empiric antibiotic coverage of atypical pathogens for community acquired pneumonia in hospitalized adults.Cochrane Database Syst. Rev.2005:CD004418.
  44. Mills GD,Oehley MR,Arrol B.Effectiveness of beta lactam antibiotics compared with antibiotics active against atypical pathogens in non‐severe community acquired pneumonia: meta‐analysis.Br Med J.2005;330:456.
  45. Lin E,Stanek RJ,Mufson MA.Lack of synergy of erythromycin combined with penicillin or cefotaxime against Streptococcus pneumoniae in vitro.Antimicrob Agents Chemother.2003;47:11511153.
  46. Johansen HK,Jensen TG,Dessau RB,Lundgren B,Frimodt‐Moller N.Antagonism between penicillin and erythromycin against Streptococcus pneumoniae in vitro and in vivo.J Antimicrob Chemother.2000;46:973980.
  47. Tamaoki J.The effects of macrolides on inflammatory cells.Chest.2004;125(2 Suppl):41S50S; quiz 1S.
  48. Ruiz M,Ewig S,Torres A, et al.Severe community‐acquired pneumonia. Risk factors and follow‐up epidemiology.Am J Respir Crit Care Med.1999;160:923929.
  49. Ewig S,Ruiz M,Mensa J, et al.Severe community‐acquired pneumonia. Assessment of severity criteria.Am J Respir Crit Care Med.1998;158:11021108.
  50. Willis BC,Ndiaye SM,Hopkins DP,Shefer A.Improving influenza, pneumococcal polysaccharide, and hepatitis B vaccination coverage among adults aged <65 years at high risk: a report on recommendations of the Task Force on Community Preventive Services.MMWR Recomm Rep.2005;54(RR‐5):111.
  51. Conaty S,Watson L,Dinnes J,Waugh N.The effectiveness of pneumococcal polysaccharide vaccines in adults: a systematic review of observational studies and comparison with results from randomised controlled trials.Vaccine.2004;22:32143224.
  52. Watson L,Wilson BJ,Waugh N.Pneumococcal polysaccharide vaccine: a systematic review of clinical effectiveness in adults.Vaccine.2002;20:21662173.
  53. Jackson LA,Neuzil KM,Yu O, et al.Effectiveness of pneumococcal polysaccharide vaccine in older adults.N Engl J Med.2003;348:17471755.
  54. Butler JC,Breiman RF,Campbell JF,Lipman HB,Broome CV,Facklam RR.Pneumococcal polysaccharide vaccine efficacy. An evaluation of current recommendations.JAMA.1993;270:18261831.
  55. Balakrishnan I,Crook P,Morris R,Gillespie SH.Early predictors of mortality in pneumococcal bacteraemia.J Infect.2000;40:256261.
  56. Afessa B,Greaves WL,Frederick WR.Pneumococcal bacteremia in adults: a 14‐year experience in an inner‐city university hospital.Clin Infect Dis.1995;21:345351.
  57. Laurichesse H,Grimaud O,Waight P,Johnson AP,George RC,Miller E.Pneumococcal bacteraemia and meningitis in England and Wales, 1993 to 1995.Commun Dis Public Health.1998;1(1):2227.
  58. Kramer MR,Rudensky B,Hadas‐Halperin I,Isacsohn M,Melzer E.Pneumococcal bacteremia—no change in mortality in 30 years: analysis of 104 cases and review of the literature.Isr J Med Sci.1987;23:174180.
  59. Dear K,Holden J,Andrews R,Tatham D.Vaccines for preventing pneumococcal infection in adults.Cochrane Database Syst Rev.2003:CD000422.
  60. Nichol KL,Baken L,Wuorenma J,Nelson A.The health and economic benefits associated with pneumococcal vaccination of elderly persons with chronic lung disease.Arch Intern Med.1999;159:24372442.
  61. Lexau CA,Lynfield R,Danila R, et al.Changing epidemiology of invasive pneumococcal disease among older adults in the era of pediatric pneumococcal conjugate vaccine.JAMA.2005;294:20432051.
  62. Whitney CG,Farley MM,Hadler J, et al.Decline in invasive pneumococcal disease after the introduction of protein‐polysaccharide conjugate vaccine.N Engl J Med.2003;348:17371746.
  63. Kyaw MH,Lynfield R,Schaffner W, et al.Effect of introduction of the pneumococcal conjugate vaccine on drug‐resistant Streptococcus pneumoniae.N Engl J Med.2006;354:14551463.
  64. Voordouw BC,van der Linden PD,Simonian S,van der Lei J,Sturkenboom MC,Stricker BH.Influenza vaccination in community‐dwelling elderly: impact on mortality and influenza‐associated morbidity.Arch Intern Med.2003;163:10891094.
  65. Hak E,Buskens E,van Essen GA, et al.Clinical effectiveness of influenza vaccination in persons younger than 65 years with high‐risk medical conditions: the PRISMA study.Arch Intern Med.2005;165:274280.
  66. Hak E,Nordin J,Wei F, et al.Influence of high‐risk medical conditions on the effectiveness of influenza vaccination among elderly members of 3 large managed‐care organizations.Clin Infect Dis.2002;35:370377.
  67. Nichol KL,Nordin J,Mullooly J,Lask R,Fillbrandt K,Iwane M.Influenza vaccination and reduction in hospitalizations for cardiac disease and stroke among the elderly.N Engl J Med.2003;348:13221332.
  68. Wongsurakiat P,Maranetra KN,Wasi C,Kositanont U,Dejsomritrutai W,Charoenratanakul S.Acute respiratory illness in patients with COPD and the effectiveness of influenza vaccination: a randomized controlled study.Chest.2004;125:20112020.
  69. Lee PY,Matchar DB,Clements DA,Huber J,Hamilton JD,Peterson ED.Economic analysis of influenza vaccination and antiviral treatment for healthy working adults.Ann Intern Med.2002;137:225331.
  70. Gross PA,Hermogenes AW,Sacks HS,Lau J,Levandowski RA.The efficacy of influenza vaccine in elderly persons. A meta‐analysis and review of the literature.Ann Intern Med.1995;123:518527.
  71. Voordouw AC,Sturkenboom MC,Dieleman JP, et al.Annual revaccination against influenza and mortality risk in community‐dwelling elderly persons.JAMA.2004;292:20892095.
  72. Mortensen EM,Coley CM,Singer DE, et al.Causes of death for patients with community‐acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team cohort study.Arch Intern Med.2002;162:10591064.
  73. Maneker AJ,Petrack EM,Krug SE.Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department.Ann Emerg Med.1995;25(1):3640.
  74. Levin KP,Hanusa BH,Rotondi A, et al.Arterial blood gas and pulse oximetry in initial management of patients with community‐acquired pneumonia.J Gen Intern Med.2001;16:590598.
  75. Law M,Tang JL.An analysis of the effectiveness of interventions intended to help people stop smoking.Arch Intern Med.1995;155:19331941.
  76. A clinical practice guideline for treating tobacco use and dependence: A US Public Health Service report.The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium Representatives.JAMA.2000;283:32443254.
  77. Rhew DC.Quality indicators for the management of pneumonia in vulnerable elders.Ann Intern Med.2001;135:736743.
  78. Nuorti JP,Butler JC,Farley MM, et al.Cigarette smoking and invasive pneumococcal disease.Active Bacterial Core Surveillance Team.N Engl J Med.2000;342:681689.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
344-353
Legacy Keywords
community‐acquired and nosocomial pneumonia, quality improvement, care standardization
Sections
Article PDF
Article PDF

The quality movement has spawned efforts to define and measure best practices for clinical conditions commonly cared for by hospitalists. Pneumonia is the most frequent infectious cause of death in the United States, and it accounts for more than 1 million hospitalizations annually at an estimated annual cost of $12.2 billion, most of it incurred by inpatients.1 The morbidity and mortality of the elderly are particularly burdensome.2, 3 For these reasons, attention has been focused on improving the quality of care of inpatients with community‐acquired pneumonia (CAP).

Credentialing agencies such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) require hospitals to report performance on predefined core measures of pneumonia care that they have identified as best practices (see Table 1).4, 5 The performance of individual organizations on these measures is now publicly reported at a website (www.hospitalcompare.hhs.gov) sponsored by the U.S. Department of Health and Human Services in conjunction with the Hospital Quality Alliance. Similar information is available at JCAHO's www.qualitycheck.org. Health care consumers can review quality data from the institution of their choice and compare the performance of various hospitals. The Centers for Medicare & Medicaid Services (CMS) provides financial incentives for the public reporting of such data and distributed $8.85 million to the top‐performing hospitals participating in a demonstration project in 2005.68 Voluntary reporting of performance on quality measures by individual physicians,9 as well as hospitals, is now being encouraged. As congress currently considers implementing pay for performance measures as a means to improve physician reimbursement, reporting will ultimately be linked to physician payments.

Core Measures of Quality Care for Pneumonia in Hospitalized Patients
  • Non‐ICU: B‐lactam + (macrolide or doxycycline) or respiratory fluoroquinolone.

  • ICU: B‐lactam + (macrolide or respiratory fluoroquinolone).

  • ICU with pseudomonal risk: IV antipseudomonal B‐lactam + (ciprofloxacin or levofloxacin) or antipseudomonal B‐lactam + aminoglycoside + ([ciprofloxacin or levofloxacin] or macrolide).

Collection of blood cultures before antibiotic therapy.
Collection of blood cultures within 24 hours of admission.
Mean time of less than 4 hours from arrival to initial administration of antibiotics.
Choice of initial antibiotics according to established guidelines.*
Pneumococcal screening and vaccination of eligible patients by discharge.
Influenza screening and vaccination of eligible patients during flu season.
Oxygenation assessment within 24 hours of admission.
Smoking cessation counseling to all smokers.

Performance on core measures for pneumonia is less consistent across hospitals than the other conditions currently being monitored.7 It is instructive, then, to review the evidence base for the existing pneumonia quality measures, which can inform decisions about prioritizing interventions to provide the most effective care for inpatients with CAP.

BLOOD CULTURES

In a large multicenter retrospective study of Medicare patients hospitalized with CAP, Meehan et al.10 found the performance of blood cultures within 24 hours of arrival to be associated with reduced 30‐day mortality. Despite the large sample size of more than 14,000 patients, the risk‐adjusted mortality reduction was of only borderline significance (RR 0.9 [0.81‐1.00]). The unadjusted data did not show a significant mortality reduction. Notably, collection of blood cultures prior to antibiotic administration did not affect mortality, even excluding patients receiving prehospital antibiotics.

A smaller review of 38 U.S. academic medical centers showed relatively high compliance with blood culture performance, but no mortality reduction, even after adjustment for severity of illness. Similarly, performing blood cultures before administration of antibiotics yielded no significant effect.11

Several studies call into question the clinical utility of performing blood cultures drawn from patients with CAP. Combined, these studies evaluated almost 3000 pneumonia patients who had blood cultures drawn; the likelihood of a change in therapy based on results was at most 5%. Among the patients with positive cultures, only 20%‐40% had a treatment change based on the result.1215

The more severely ill patients with CAP may benefit from blood cultures, though the findings reported in the literature vary.12, 16 Using the Pneumonia Severity Index (PSI) score17 to classify severity of illness, an observational study of 209 inpatients with CAP found the yield of blood cultures increased from 10% in the lowest‐risk groups to 27% in the most severely ill.16 In contrast, two larger studies with a combined enrollment of almost 14,000 patients were unable to demonstrate a difference in the incidence of bacteremia despite adjustment for the PSI score.12, 18 It is clear from these and other studies that patients in PSI classes I‐III derive very little benefit from the performance of blood cultures.12, 16, 19

Metersky et al.18 described a prospectively validated risk assessment tool that reliably predicted bacteremia in Medicare patients with CAP and explored its utility in reducing unnecessary blood cultures. Independent risk factors for bacteremia included prior antibiotic use, liver disease, hypotension, tachycardia, fever or hypothermia, BUN > 30 mg/dL, sodium < 130 mmol/L, and WBC < 5000 or > 20,000/mm2. Use of this tool predicted bacteremia in 89% of patients and avoided 39% of unnecessary blood cultures. The authors also tested a modified version of the tool that excluded the laboratory abnormalities, so rapid assessment could be made at the initial patient presentation. This version advocated a single blood culture for most patients, and 2 blood cultures for patients with 2 or more risk factors. The modified tool accurately identified 88% of the patients with bacteremia and enabled a 44% reduction in unnecessary cultures.

In summary, blood cultures occasionally provide useful clinical information about etiology and resistance patterns, but they do not seem to reliably influence therapeutic decisions. It seems inappropriate to recommend against their use in practice, but they are not a solid benchmark for evidence‐based quality care. Measures that mandate risk assessment of all inpatients with CAP and require blood cultures only for older patients or those judged at high risk by PSI may better reflect quality. Alternatively, performing blood cultures on patients deemed to be high risk by the model of Metersky et al.18 may suffice.

ANTIBIOTIC TIMING

In a study of Medicare patients by Meehan et al.,10 the 30‐day mortality rate was reduced by 15% in the subset of patients who received antibiotics within 8 hours of arrival at the hospital. However, a trend toward mortality reduction was noted for those receiving antibiotics as early as 6 hours after arrival. Rapid administration of antibiotics was thus deemed an important measure of the quality of care of patients with CAP.

Additional studies attempted to confirm this observation. Battleman et al.20 evaluated 700 patients admitted for CAP through the emergency department. They found that a delay of more than 8 hours in the administration of antibiotics was correlated with a prolonged inpatient stay. Mortality rates were not reported. Achieving rapid delivery of antibiotics was closely linked to administration of the first dose of antibiotics in the emergency department.

Conversely, a large retrospective review by Dedier et al.11 found no reduction in inpatient mortality or in length of stay based on rapid antibiotic delivery, despite adjustment for severity of illness. They did not evaluate 30‐day mortality.

The effect of antibiotic timing on the time to clinical stability has also been investigated. Clinical stability was defined as 24 hours of a systolic blood pressure 90 mm Hg, heart rate 100 beats/min, respiratory rate 24 breaths/min, temperature 38.3C (101F), room air oxygen saturation 90%, and the ability to eat. Silber et al.,21 in a review of the records of 409 inpatients with moderate to severe CAP by PSI score, compared patients receiving antibiotics less than 4 hours, between 4 and 8 hours, and more than 8 hours after hospital admission. There was no difference between groups in time to clinical stability, even with adjustment for PSI.

Marrie and Wu22 attempted to define the factors that influenced inpatient mortality of patients with CAP not admitted to the intensive care unit (ICU). In a prospective study of 3043 patients evaluating a clinical pathway, a multivariate analysis showed antibiotic administration within 4 hours was not correlated with reduced mortality.

Although most studies supporting rapid antibiotic delivery used a target of 8 hours, administration in less than 4 hours is the consensus standard for pneumonia care set by CMS and JCAHO.23, 24

A benefit of timing antibiotic administration less than 4 hours after admission has been confirmed by a single, very large retrospective study of Medicare patients at least 65 years old.25 Analysis of a random sample of more than 18,000 patients with CAP who had not received prehospital antibiotics showed that the relative risk reduction for inpatient mortality was 15% in the group receiving antibiotics within 4 hours. Thirty‐day mortality was similarly reduced, and benefits continued for every hour of early antibiotic administration up to 9 hours.

The absolute risk reduction was small, however (0.6%), yielding a number needed to treat of 167 patients to prevent 1 death.

Randomized controlled trials, which would more definitively address the issue of antibiotic timing, are unlikely, as intentionally delaying administration of antibiotics to patients with known CAP is unethical. Hence, reliance on observational data must suffice. Intuitively, it makes sense to begin treatment of a bacterial infection at the earliest time possible. However, it is also known that not all patients present in a typical fashion, and diagnosis is uncertain at least 20% of the time.26 Anecdotal reports suggest that incentivizing physicians on performance measures encourages premature administration of empiric antibiotics to all patients presenting with cough, prior to confirmation of pneumonia.27, 28 Such practices promote further antibiotic resistance, arguably a larger health issue than delay in antibiotic delivery.29, 30

Houck31 offers potential solutions to this problem, such as eliminating the pressure on hospitals to perform at 100% on this measure by reporting performance within acceptable ranges (eg, 70%‐84% and 85%‐100%) Targeting a benchmark of 80% or a duration of 6 hours may also be appropriate. Finally, a 4‐hour benchmark has not been shown to benefit younger patients, so it is important to apply this target only to patients more than 65 years of age.

CHOICE OF ANTIBIOTIC

A retrospective review of 12,945 cases of inpatients with CAP found that, in comparison to ceftriaxone alone, initial antibiotic regimens consisting either of a second‐ or third‐generation cephalosporin plus a macrolide or of a fluoroquinolone alone were associated with an approximately 30% reduction in 30‐day mortality.32 Hence, current guidelines recommend the combination of a B‐lactam and macrolide, a B‐lactam and doxycycline, or a respiratory fluoroquinolone for inpatients with CAP not admitted to the ICU.3335

The results of subsequent studies supported the contention that guideline‐compliant antibiotics improve outcomes. A prospective multicenter study of a clinical pathway that encouraged use of either levofloxacin or cefuroxime plus azithromycin for the initial treatment of inpatient CAP showed significantly reduced mortality. Compared with any other antibiotic regimen, the odds ratio for death was 0.22 with the cephalosporin/macrolide combination and 0.43 with the fluoroquinolone. Of note, early mortality (within 5 days of admission) was not reduced by antibiotic choice.22 Similar results were found in a retrospective analysis, which found the odds of 30‐day mortality increased by 5.7 in patients not receiving guideline‐compliant therapy.36 A third study found guideline‐compliant antibiotics reduced the likelihood of a prolonged length of stay by 45%.20

Of note, data on the effectiveness of the cephalosporin/doxycycline combination are limited, and the major guidelines differ about whether this regimen is appropriate for inpatients with CAP.33, 34 Important findings from a recent retrospective cohort study showed that initial therapy with ceftriaxone plus doxycycline was associated with reduced inpatient mortality (OR = 0.26) as well as reduced 30‐day mortality (OR = 0.37) compared with other guideline‐compliant therapies for CAP.37 When patients who would not have been considered appropriate for initial doxycycline therapy (those resident in nursing homes, with aspiration pneumonia, or in the ICU) were excluded, a large reduction in inpatient mortality remained (OR = 0.17), without any increase in length of stay or readmission rate. Interestingly, this study suggests the potential superiority of this regimen, though a randomized controlled trial is needed to confirm this. The current core measures do include doxycycline as an acceptable option for CAP therapy (see Table 1).

Currently, controversy remains about whether the benefit of these selected regimens results from their activity against atypical pathogens (Mycoplasma, Legionella, Chlamydia) and whether there is additional benefit from using combination antibiotic therapy.38, 39 Waterer40 described 225 inpatients with bacteremic pneumococcal pneumonia, noting the antibiotic regimen received during the first 24 hours of hospitalization. Patients were classified retrospectively into 3 groupssingle effective therapy (SET), dual effective therapy (DET), or more than dual effective therapy (MET)on the basis of the concordance of pneumococcal sensitivity with the initial antibiotics. Patients on 2 antibiotics were classified in the DET group if the organism was sensitive to both and in the SET group if the organism was resistant to 1 of the 2. Those in the MET group were analyzed separately, as they were found to have a higher baseline severity of illness based on the PSI score; the SET and DET groups were equivalent.

Surprisingly, the SET group was found to have a 3‐fold increase in inpatient mortality; adjustment for severity of illness increased the odds ratio for death to 6.4. Of note, all deaths were in the most severely ill patients (PSI IV‐V). The protective effects of receiving DET were not specifically limited to those receiving a macrolide as the second agent, and multivariate analysis did not find coverage of atypical organisms to be an independent predictor of mortality.

A recent prospective multicenter trial of 844 patients with bacteremic pneumococcal pneumonia at 21 hospitals confirmed these findings.41 A significant 14‐day survival advantage (23% versus 55%) was found in the subgroup of critically ill patients who received at least 2 effective antibiotics. Though survival benefit was restricted to the sickest patients, severity of illness was similar among the groups.

The specific importance of macrolides in combination therapy remains under investigation. A review of a database of inpatients with bacteremic pneumococcal pneumonia over a 10‐year period found that 58% received initial empiric therapy with a B‐lactam/macrolide combination and 42% received B‐lactam without a macrolide (though other antibiotic combinations were not excluded).42 After logistic regression analysis, the investigators found a relative reduction in inpatient mortality of 60% in the patients receiving combination therapy with macrolides. Unfortunately, neither comparison to fluoroquinolone monotherapy nor risk stratification by PSI was reported. A similar study from Canada that did stratify for risk confirmed a mortality benefit of combination therapy.43

A subsequent, extremely large study of more than 44,000 patients from a hospital claims‐made database lent support to these findings.44 This study included all CAP patients regardless of microbiology and was not restricted to those with bacteremia. Outcomes among groups receiving monotherapy with any of the standard agents for CAP were compared with those in groups receiving combination therapy with a macrolide as the second agent. Statistically significant reductions in 30‐day mortality were observed in all groups receiving dual therapy with macrolides. Consistent with other studies, the benefit applied only to patients with more severe CAP. The percentage of patients with bacteremia was not specified.

Of note, this study did not allow direct comparison of fluoroquinolone monotherapy to combination therapy with a B‐lactam and a macrolide. However, the fluoroquinolone/macrolide combination conferred no additional benefit beyond fluoroquinolone monotherapy when adjusted for severity of illness or age. This implies that fluoroquinolone monotherapy is adequate, at least in some subpopulations. This is consistent with initial studies that established the superiority of the antibiotic combinations recommended by the guidelines.20, 22, 32

The potential benefit of combination therapy appears limited to patients with higher severity of illness and pneumococcal bacteremia. However, outcomes are affected by the antibiotic regimen selected in the initial 24‐48 hours of hospitalization, before results of blood cultures are routinely available. At present, clinical prediction of patients who will benefit from combination therapy is difficult.

Coverage of undiagnosed mixed infections with atypical organisms is probably not a major factor benefiting patients receiving combination therapy. Several recent meta‐analyses found no reduction in mortality or the rate of clinical failure among patients receiving antibiotics covering atypical organisms compared with those for patients whose regimens did not have such coverage.4547 Subgroups of patients with Legionella pneumonia do benefit from antibiotics with targeted activity against atypical organisms, but fewer than 1% of all patients were so identified. Evidence for antibiotic synergy is similarly lacking.48, 49 The immunomodulatory effects of macrolides, which decrease cytokine production and inflammation and subsequently reduce the severity of lung injury and other complications of sepsis, are considered potential factors in the reduction of mortality.50

The definition of severe CAP and the indications for ICU admission remain controversial, evidence for which is reviewed elsewhere.34, 51, 52 Antibiotic recommendations for ICU patients are included in Table 1 for completeness, but a detailed review of the evidence is lacking because current guidelines are based on consensus opinion.34 The use of fluoroquinolone monotherapy in severe CAP is not currently recommended because of limitations of the existing evidence. The majority of quinolone trials have excluded severely ill patients, and approval trials of newer respiratory fluoroquinolones have used levofloxacin as a comparator. Studies comparing fluoroquinolones typically allowed investigators in the B‐lactam arm the option of adding macrolides or tetracycline at their discretion. In addition, such trials have been designed as noniferiority trials.38 Clearly, randomized controlled trials are needed to resolve this issue.

Currently, selecting appropriate antibiotics should follow established guidelines, with consideration of using combination therapy for patients with a higher severity of illness. Emphasis on this measure should be stronger than that on antibiotic timing, as the bulk of the evidence favors significant mortality reduction from following guidelines for antibiotic therapy.

VACCINATION

Guidelines recommend all eligible adults hospitalized with CAP receive pneumococcal vaccination on discharge,3335, 53 though there is no evidence this reduces the incidence of pneumonia or death.54, 55 Retrospective studies have shown reduced incidence of invasive disease (bacteremia and meningitis), but not of other end points.5457 The estimated mortality from pneumococcal bacteremia remain as high as 20%‐30%, with no evidence that this rate has decreased over the last 30 years.5861 Despite this, a recent meta‐analysis from the Cochrane database that included only randomized, controlled trials (75,197 patients in 15 trials) was unable to show significant reductions in all‐cause pneumonia or mortality for vaccinated subjects.62 Cohort studies, evaluated separately in this analysis, showed an efficacy of 53% in reducing the incidence of invasive pneumococcal disease. Given the relatively low incidence of invasive disease in the general population, the number needed to treat was estimated at 20,000, or 4000 if only older patients were considered. A subsequent retrospective cohort study showed no reduction in pneumonia hospitalizations, cases of outpatient pneumonia, or mortality among 45,365 elderly vaccinees.56 Some specific subgroups may benefit, however. Vaccinated patients with chronic lung disease did show a reduction in hospitalization for pneumonia (RR 0.57 [0.38‐0.84]) and in mortality (RR 0.7 [0.56‐0.9]) in a retrospective study of HMO patients older than age 65.63

It is of interest that since the licensure of the pediatric 7‐valent protein‐polysaccharide conjugate vaccine in 2000, the incidence of invasive pneumococcal disease among adults has dropped significantly. Overall reduction in invasive disease in adults more than 50 years old was 11% from 1998 to 2003 (relative risk reduction [RRR] = 28%). This is likely the result of decreased transmission from colonized or infected children and not a coincidental increase in adult pneumococcal vaccination, as the rates of disease caused by the 16 strains unique to the 23‐valent vaccine did not change.64, 65 The overall reduction in the incidence of invasive disease is still superior with the adult vaccine, up to 30% in vaccinated subjects (RRR = 44%).56 Invasive disease caused specifically by penicillin‐nonsusceptible serotypes has dropped by 49% in the elderly since introduction of the vaccine.66 Thus, the combined impact of the 2 vaccines may be significant. It is not yet clear what effect, if any, the 7‐valent vaccine will have on the hospitalization rate or mortality.

In contrast to the results for pneumococcal vaccination, studies of the benefits of influenza vaccination have shown clear and consistent reductions in mortality, respiratory illness, hospitalization, and pneumonia, especially among patients with comorbidities.6771 Cost effectiveness has been demonstrated for all populations,72, 73 and the reduction in mortality among high‐risk patients younger than age 65 has been estimated to be as high as 78%.68 Among the elderly, reduction in mortality of about 50% has been reported, along with 20%‐30% reductions in hospitalizations for pneumonia, influenza, cardiac disease, and stroke.70 Reduced incidence of pneumonia in vaccinated patients has even been documented among elderly patients without specific comorbidities.67 Annual revaccination has the most significant impact on mortality.74

The pneumococcal vaccine remains important in the effort to reduce the severity of and complications from invasive pneumococcal disease in the elderly, but the lack of significant benefits on hard end points such as mortality or hospitalizations makes it a less robust measure of quality pneumonia care. In contrast, influenza vaccination has a much larger impact on outcomes in the population at risk. Emphasis should be shifted from pneumococcal to influenza vaccine in pneumonia performance measures.

OXYGENATION ASSESSMENT

It seems intuitive that oxygenation assessment is important in the initial evaluation of patients with CAP, though there is not direct evidence to support this. The recommendation for oxygenation assessment in the published guidelines for CAP is by consensus.3335 Documented hypoxemia is associated with increased pneumonia‐related mortality,17, 75 and clinical judgment does not adequately predict hypoxemia.76 Though the assessment of oxygenation has been found to vary widely among practitioners,77 performance has remained consistent since the advent of monitoring and reporting of quality measures, with compliance rates of 99%.4, 7 Monitoring performance of this measure should continue, though high compliance rates limit its ability to discriminate among institutions.

SMOKING CESSATION COUNSELING

Counseling patients to stop smoking was found to be modestly (2%) but statistically significantly effective in promoting abstinence at 1 year.78 In its report on treating tobacco use, the U.S. Public Health Services recommended that all smokers receive hospital‐ and system‐based interventions at every visit.79 As part of the Pneumonia Patient Outcomes Research Team (PORT) study, smokers with pneumonia underwent a tobacco cessation interview. Though only 15% of these patients quit smoking, 93% of those who quit did so at the time they developed CAP.80 A retrospective study of patients with bacteremic pneumococcal pneumonia found tobacco exposure, including passive smoking, to be a strong independent risk factor for invasive disease.81 The most recent CAP guidelines from the Infectious Disease Society of America (IDSA) recommend smoking cessation counseling for all hospitalized patients who smoke.33 However, hospitals are not likely to have the impact that a more comprehensive, outpatient‐based smoking cessation program would. Without ongoing support, counseling, and pharmacotherapy, the effects of an intervention would be expected to be small.79 Though evidence of benefit is limited, smoking cessation interventions should be encouraged at all sites of care. Quality care merits this regardless of admitting diagnosis, but benefits specific to CAP outcomes have not yet been demonstrated.

CONCLUSIONS

The burden of illness caused by CAP mandates that clinicians strive to deliver the highest quality of care to afflicted patients. Critical evaluation of the strength of the evidence will continue to guide such endeavors, and changes in practice will follow as new information surfaces. Standards of care, as adopted by consensus groups such as the IDSA and American Thoracic Society, will continue to inform the practice of hospitalists.

How quality is defined for public reporting requires particularly careful assessment. The definition of quality should be based on evidence more rigorous than that ascribed to consensus guidelines. Within the profession, guidelines offer reasonable standards of care and delineate areas for further research and are invaluable tools for practicing clinicians. In the public arena, however, proclaiming practices as good or bad sets expectations of health care consumers not educated in the nuances of evaluating clinical evidence and can unfairly bias them against conscientious and effective providers whose standards reflect different interpretations of controversial issues. Regulatory agencies should publicly target interventions using only the most solid evidentiary foundation while internally striving to monitor the effects of different practice patterns and report measurable differences in outcomes revealed by careful investigation. Areas where controversy remains should be the primary targets of further research but should not be offered as benchmarks for public scrutiny until the medical community has settled on a position.

Furthermore, when evidence remains questionable, financial incentives should be linked to performance indicators with extreme caution. It would be counterproductive if health care organizations, driven to achieve optimal antibiotic timing to obtain payment updates from CMS, began to administer antibiotics prior to completing workups on all patients with respiratory complaints, as this would likely lead to antibiotic overuse. Similarly, institutions pushed to collect blood cultures before antibiotics are given may inappropriately delay administration in order to perform well on quality measures, resulting in potential harm to patients.

The measures of quality care for CAP for which the evidence on outcomes is the most convincing are antibiotic selection (mortality benefit, reduction in LOS) and influenza vaccination (mortality benefit, reduction in hospitalizations, reduction in respiratory illness). Antibiotic timing also shows a smaller but convincing reduction in mortality, though the advantages of receiving antibiotics within 4 hours instead of 8 hours are not clearly established for younger patients. These measures should be emphasized most heavily in the arena of public reporting and incentives for quality care, with additions and modifications guided by emerging evidence. Revision of the other measures to conform with current evidence would allow public reporting to more accurately reflect quality.

The quality movement has spawned efforts to define and measure best practices for clinical conditions commonly cared for by hospitalists. Pneumonia is the most frequent infectious cause of death in the United States, and it accounts for more than 1 million hospitalizations annually at an estimated annual cost of $12.2 billion, most of it incurred by inpatients.1 The morbidity and mortality of the elderly are particularly burdensome.2, 3 For these reasons, attention has been focused on improving the quality of care of inpatients with community‐acquired pneumonia (CAP).

Credentialing agencies such as the Joint Commission on Accreditation of Healthcare Organizations (JCAHO) require hospitals to report performance on predefined core measures of pneumonia care that they have identified as best practices (see Table 1).4, 5 The performance of individual organizations on these measures is now publicly reported at a website (www.hospitalcompare.hhs.gov) sponsored by the U.S. Department of Health and Human Services in conjunction with the Hospital Quality Alliance. Similar information is available at JCAHO's www.qualitycheck.org. Health care consumers can review quality data from the institution of their choice and compare the performance of various hospitals. The Centers for Medicare & Medicaid Services (CMS) provides financial incentives for the public reporting of such data and distributed $8.85 million to the top‐performing hospitals participating in a demonstration project in 2005.68 Voluntary reporting of performance on quality measures by individual physicians,9 as well as hospitals, is now being encouraged. As congress currently considers implementing pay for performance measures as a means to improve physician reimbursement, reporting will ultimately be linked to physician payments.

Core Measures of Quality Care for Pneumonia in Hospitalized Patients
  • Non‐ICU: B‐lactam + (macrolide or doxycycline) or respiratory fluoroquinolone.

  • ICU: B‐lactam + (macrolide or respiratory fluoroquinolone).

  • ICU with pseudomonal risk: IV antipseudomonal B‐lactam + (ciprofloxacin or levofloxacin) or antipseudomonal B‐lactam + aminoglycoside + ([ciprofloxacin or levofloxacin] or macrolide).

Collection of blood cultures before antibiotic therapy.
Collection of blood cultures within 24 hours of admission.
Mean time of less than 4 hours from arrival to initial administration of antibiotics.
Choice of initial antibiotics according to established guidelines.*
Pneumococcal screening and vaccination of eligible patients by discharge.
Influenza screening and vaccination of eligible patients during flu season.
Oxygenation assessment within 24 hours of admission.
Smoking cessation counseling to all smokers.

Performance on core measures for pneumonia is less consistent across hospitals than the other conditions currently being monitored.7 It is instructive, then, to review the evidence base for the existing pneumonia quality measures, which can inform decisions about prioritizing interventions to provide the most effective care for inpatients with CAP.

BLOOD CULTURES

In a large multicenter retrospective study of Medicare patients hospitalized with CAP, Meehan et al.10 found the performance of blood cultures within 24 hours of arrival to be associated with reduced 30‐day mortality. Despite the large sample size of more than 14,000 patients, the risk‐adjusted mortality reduction was of only borderline significance (RR 0.9 [0.81‐1.00]). The unadjusted data did not show a significant mortality reduction. Notably, collection of blood cultures prior to antibiotic administration did not affect mortality, even excluding patients receiving prehospital antibiotics.

A smaller review of 38 U.S. academic medical centers showed relatively high compliance with blood culture performance, but no mortality reduction, even after adjustment for severity of illness. Similarly, performing blood cultures before administration of antibiotics yielded no significant effect.11

Several studies call into question the clinical utility of performing blood cultures drawn from patients with CAP. Combined, these studies evaluated almost 3000 pneumonia patients who had blood cultures drawn; the likelihood of a change in therapy based on results was at most 5%. Among the patients with positive cultures, only 20%‐40% had a treatment change based on the result.1215

The more severely ill patients with CAP may benefit from blood cultures, though the findings reported in the literature vary.12, 16 Using the Pneumonia Severity Index (PSI) score17 to classify severity of illness, an observational study of 209 inpatients with CAP found the yield of blood cultures increased from 10% in the lowest‐risk groups to 27% in the most severely ill.16 In contrast, two larger studies with a combined enrollment of almost 14,000 patients were unable to demonstrate a difference in the incidence of bacteremia despite adjustment for the PSI score.12, 18 It is clear from these and other studies that patients in PSI classes I‐III derive very little benefit from the performance of blood cultures.12, 16, 19

Metersky et al.18 described a prospectively validated risk assessment tool that reliably predicted bacteremia in Medicare patients with CAP and explored its utility in reducing unnecessary blood cultures. Independent risk factors for bacteremia included prior antibiotic use, liver disease, hypotension, tachycardia, fever or hypothermia, BUN > 30 mg/dL, sodium < 130 mmol/L, and WBC < 5000 or > 20,000/mm2. Use of this tool predicted bacteremia in 89% of patients and avoided 39% of unnecessary blood cultures. The authors also tested a modified version of the tool that excluded the laboratory abnormalities, so rapid assessment could be made at the initial patient presentation. This version advocated a single blood culture for most patients, and 2 blood cultures for patients with 2 or more risk factors. The modified tool accurately identified 88% of the patients with bacteremia and enabled a 44% reduction in unnecessary cultures.

In summary, blood cultures occasionally provide useful clinical information about etiology and resistance patterns, but they do not seem to reliably influence therapeutic decisions. It seems inappropriate to recommend against their use in practice, but they are not a solid benchmark for evidence‐based quality care. Measures that mandate risk assessment of all inpatients with CAP and require blood cultures only for older patients or those judged at high risk by PSI may better reflect quality. Alternatively, performing blood cultures on patients deemed to be high risk by the model of Metersky et al.18 may suffice.

ANTIBIOTIC TIMING

In a study of Medicare patients by Meehan et al.,10 the 30‐day mortality rate was reduced by 15% in the subset of patients who received antibiotics within 8 hours of arrival at the hospital. However, a trend toward mortality reduction was noted for those receiving antibiotics as early as 6 hours after arrival. Rapid administration of antibiotics was thus deemed an important measure of the quality of care of patients with CAP.

Additional studies attempted to confirm this observation. Battleman et al.20 evaluated 700 patients admitted for CAP through the emergency department. They found that a delay of more than 8 hours in the administration of antibiotics was correlated with a prolonged inpatient stay. Mortality rates were not reported. Achieving rapid delivery of antibiotics was closely linked to administration of the first dose of antibiotics in the emergency department.

Conversely, a large retrospective review by Dedier et al.11 found no reduction in inpatient mortality or in length of stay based on rapid antibiotic delivery, despite adjustment for severity of illness. They did not evaluate 30‐day mortality.

The effect of antibiotic timing on the time to clinical stability has also been investigated. Clinical stability was defined as 24 hours of a systolic blood pressure 90 mm Hg, heart rate 100 beats/min, respiratory rate 24 breaths/min, temperature 38.3C (101F), room air oxygen saturation 90%, and the ability to eat. Silber et al.,21 in a review of the records of 409 inpatients with moderate to severe CAP by PSI score, compared patients receiving antibiotics less than 4 hours, between 4 and 8 hours, and more than 8 hours after hospital admission. There was no difference between groups in time to clinical stability, even with adjustment for PSI.

Marrie and Wu22 attempted to define the factors that influenced inpatient mortality of patients with CAP not admitted to the intensive care unit (ICU). In a prospective study of 3043 patients evaluating a clinical pathway, a multivariate analysis showed antibiotic administration within 4 hours was not correlated with reduced mortality.

Although most studies supporting rapid antibiotic delivery used a target of 8 hours, administration in less than 4 hours is the consensus standard for pneumonia care set by CMS and JCAHO.23, 24

A benefit of timing antibiotic administration less than 4 hours after admission has been confirmed by a single, very large retrospective study of Medicare patients at least 65 years old.25 Analysis of a random sample of more than 18,000 patients with CAP who had not received prehospital antibiotics showed that the relative risk reduction for inpatient mortality was 15% in the group receiving antibiotics within 4 hours. Thirty‐day mortality was similarly reduced, and benefits continued for every hour of early antibiotic administration up to 9 hours.

The absolute risk reduction was small, however (0.6%), yielding a number needed to treat of 167 patients to prevent 1 death.

Randomized controlled trials, which would more definitively address the issue of antibiotic timing, are unlikely, as intentionally delaying administration of antibiotics to patients with known CAP is unethical. Hence, reliance on observational data must suffice. Intuitively, it makes sense to begin treatment of a bacterial infection at the earliest time possible. However, it is also known that not all patients present in a typical fashion, and diagnosis is uncertain at least 20% of the time.26 Anecdotal reports suggest that incentivizing physicians on performance measures encourages premature administration of empiric antibiotics to all patients presenting with cough, prior to confirmation of pneumonia.27, 28 Such practices promote further antibiotic resistance, arguably a larger health issue than delay in antibiotic delivery.29, 30

Houck31 offers potential solutions to this problem, such as eliminating the pressure on hospitals to perform at 100% on this measure by reporting performance within acceptable ranges (eg, 70%‐84% and 85%‐100%) Targeting a benchmark of 80% or a duration of 6 hours may also be appropriate. Finally, a 4‐hour benchmark has not been shown to benefit younger patients, so it is important to apply this target only to patients more than 65 years of age.

CHOICE OF ANTIBIOTIC

A retrospective review of 12,945 cases of inpatients with CAP found that, in comparison to ceftriaxone alone, initial antibiotic regimens consisting either of a second‐ or third‐generation cephalosporin plus a macrolide or of a fluoroquinolone alone were associated with an approximately 30% reduction in 30‐day mortality.32 Hence, current guidelines recommend the combination of a B‐lactam and macrolide, a B‐lactam and doxycycline, or a respiratory fluoroquinolone for inpatients with CAP not admitted to the ICU.3335

The results of subsequent studies supported the contention that guideline‐compliant antibiotics improve outcomes. A prospective multicenter study of a clinical pathway that encouraged use of either levofloxacin or cefuroxime plus azithromycin for the initial treatment of inpatient CAP showed significantly reduced mortality. Compared with any other antibiotic regimen, the odds ratio for death was 0.22 with the cephalosporin/macrolide combination and 0.43 with the fluoroquinolone. Of note, early mortality (within 5 days of admission) was not reduced by antibiotic choice.22 Similar results were found in a retrospective analysis, which found the odds of 30‐day mortality increased by 5.7 in patients not receiving guideline‐compliant therapy.36 A third study found guideline‐compliant antibiotics reduced the likelihood of a prolonged length of stay by 45%.20

Of note, data on the effectiveness of the cephalosporin/doxycycline combination are limited, and the major guidelines differ about whether this regimen is appropriate for inpatients with CAP.33, 34 Important findings from a recent retrospective cohort study showed that initial therapy with ceftriaxone plus doxycycline was associated with reduced inpatient mortality (OR = 0.26) as well as reduced 30‐day mortality (OR = 0.37) compared with other guideline‐compliant therapies for CAP.37 When patients who would not have been considered appropriate for initial doxycycline therapy (those resident in nursing homes, with aspiration pneumonia, or in the ICU) were excluded, a large reduction in inpatient mortality remained (OR = 0.17), without any increase in length of stay or readmission rate. Interestingly, this study suggests the potential superiority of this regimen, though a randomized controlled trial is needed to confirm this. The current core measures do include doxycycline as an acceptable option for CAP therapy (see Table 1).

Currently, controversy remains about whether the benefit of these selected regimens results from their activity against atypical pathogens (Mycoplasma, Legionella, Chlamydia) and whether there is additional benefit from using combination antibiotic therapy.38, 39 Waterer40 described 225 inpatients with bacteremic pneumococcal pneumonia, noting the antibiotic regimen received during the first 24 hours of hospitalization. Patients were classified retrospectively into 3 groupssingle effective therapy (SET), dual effective therapy (DET), or more than dual effective therapy (MET)on the basis of the concordance of pneumococcal sensitivity with the initial antibiotics. Patients on 2 antibiotics were classified in the DET group if the organism was sensitive to both and in the SET group if the organism was resistant to 1 of the 2. Those in the MET group were analyzed separately, as they were found to have a higher baseline severity of illness based on the PSI score; the SET and DET groups were equivalent.

Surprisingly, the SET group was found to have a 3‐fold increase in inpatient mortality; adjustment for severity of illness increased the odds ratio for death to 6.4. Of note, all deaths were in the most severely ill patients (PSI IV‐V). The protective effects of receiving DET were not specifically limited to those receiving a macrolide as the second agent, and multivariate analysis did not find coverage of atypical organisms to be an independent predictor of mortality.

A recent prospective multicenter trial of 844 patients with bacteremic pneumococcal pneumonia at 21 hospitals confirmed these findings.41 A significant 14‐day survival advantage (23% versus 55%) was found in the subgroup of critically ill patients who received at least 2 effective antibiotics. Though survival benefit was restricted to the sickest patients, severity of illness was similar among the groups.

The specific importance of macrolides in combination therapy remains under investigation. A review of a database of inpatients with bacteremic pneumococcal pneumonia over a 10‐year period found that 58% received initial empiric therapy with a B‐lactam/macrolide combination and 42% received B‐lactam without a macrolide (though other antibiotic combinations were not excluded).42 After logistic regression analysis, the investigators found a relative reduction in inpatient mortality of 60% in the patients receiving combination therapy with macrolides. Unfortunately, neither comparison to fluoroquinolone monotherapy nor risk stratification by PSI was reported. A similar study from Canada that did stratify for risk confirmed a mortality benefit of combination therapy.43

A subsequent, extremely large study of more than 44,000 patients from a hospital claims‐made database lent support to these findings.44 This study included all CAP patients regardless of microbiology and was not restricted to those with bacteremia. Outcomes among groups receiving monotherapy with any of the standard agents for CAP were compared with those in groups receiving combination therapy with a macrolide as the second agent. Statistically significant reductions in 30‐day mortality were observed in all groups receiving dual therapy with macrolides. Consistent with other studies, the benefit applied only to patients with more severe CAP. The percentage of patients with bacteremia was not specified.

Of note, this study did not allow direct comparison of fluoroquinolone monotherapy to combination therapy with a B‐lactam and a macrolide. However, the fluoroquinolone/macrolide combination conferred no additional benefit beyond fluoroquinolone monotherapy when adjusted for severity of illness or age. This implies that fluoroquinolone monotherapy is adequate, at least in some subpopulations. This is consistent with initial studies that established the superiority of the antibiotic combinations recommended by the guidelines.20, 22, 32

The potential benefit of combination therapy appears limited to patients with higher severity of illness and pneumococcal bacteremia. However, outcomes are affected by the antibiotic regimen selected in the initial 24‐48 hours of hospitalization, before results of blood cultures are routinely available. At present, clinical prediction of patients who will benefit from combination therapy is difficult.

Coverage of undiagnosed mixed infections with atypical organisms is probably not a major factor benefiting patients receiving combination therapy. Several recent meta‐analyses found no reduction in mortality or the rate of clinical failure among patients receiving antibiotics covering atypical organisms compared with those for patients whose regimens did not have such coverage.4547 Subgroups of patients with Legionella pneumonia do benefit from antibiotics with targeted activity against atypical organisms, but fewer than 1% of all patients were so identified. Evidence for antibiotic synergy is similarly lacking.48, 49 The immunomodulatory effects of macrolides, which decrease cytokine production and inflammation and subsequently reduce the severity of lung injury and other complications of sepsis, are considered potential factors in the reduction of mortality.50

The definition of severe CAP and the indications for ICU admission remain controversial, evidence for which is reviewed elsewhere.34, 51, 52 Antibiotic recommendations for ICU patients are included in Table 1 for completeness, but a detailed review of the evidence is lacking because current guidelines are based on consensus opinion.34 The use of fluoroquinolone monotherapy in severe CAP is not currently recommended because of limitations of the existing evidence. The majority of quinolone trials have excluded severely ill patients, and approval trials of newer respiratory fluoroquinolones have used levofloxacin as a comparator. Studies comparing fluoroquinolones typically allowed investigators in the B‐lactam arm the option of adding macrolides or tetracycline at their discretion. In addition, such trials have been designed as noniferiority trials.38 Clearly, randomized controlled trials are needed to resolve this issue.

Currently, selecting appropriate antibiotics should follow established guidelines, with consideration of using combination therapy for patients with a higher severity of illness. Emphasis on this measure should be stronger than that on antibiotic timing, as the bulk of the evidence favors significant mortality reduction from following guidelines for antibiotic therapy.

VACCINATION

Guidelines recommend all eligible adults hospitalized with CAP receive pneumococcal vaccination on discharge,3335, 53 though there is no evidence this reduces the incidence of pneumonia or death.54, 55 Retrospective studies have shown reduced incidence of invasive disease (bacteremia and meningitis), but not of other end points.5457 The estimated mortality from pneumococcal bacteremia remain as high as 20%‐30%, with no evidence that this rate has decreased over the last 30 years.5861 Despite this, a recent meta‐analysis from the Cochrane database that included only randomized, controlled trials (75,197 patients in 15 trials) was unable to show significant reductions in all‐cause pneumonia or mortality for vaccinated subjects.62 Cohort studies, evaluated separately in this analysis, showed an efficacy of 53% in reducing the incidence of invasive pneumococcal disease. Given the relatively low incidence of invasive disease in the general population, the number needed to treat was estimated at 20,000, or 4000 if only older patients were considered. A subsequent retrospective cohort study showed no reduction in pneumonia hospitalizations, cases of outpatient pneumonia, or mortality among 45,365 elderly vaccinees.56 Some specific subgroups may benefit, however. Vaccinated patients with chronic lung disease did show a reduction in hospitalization for pneumonia (RR 0.57 [0.38‐0.84]) and in mortality (RR 0.7 [0.56‐0.9]) in a retrospective study of HMO patients older than age 65.63

It is of interest that since the licensure of the pediatric 7‐valent protein‐polysaccharide conjugate vaccine in 2000, the incidence of invasive pneumococcal disease among adults has dropped significantly. Overall reduction in invasive disease in adults more than 50 years old was 11% from 1998 to 2003 (relative risk reduction [RRR] = 28%). This is likely the result of decreased transmission from colonized or infected children and not a coincidental increase in adult pneumococcal vaccination, as the rates of disease caused by the 16 strains unique to the 23‐valent vaccine did not change.64, 65 The overall reduction in the incidence of invasive disease is still superior with the adult vaccine, up to 30% in vaccinated subjects (RRR = 44%).56 Invasive disease caused specifically by penicillin‐nonsusceptible serotypes has dropped by 49% in the elderly since introduction of the vaccine.66 Thus, the combined impact of the 2 vaccines may be significant. It is not yet clear what effect, if any, the 7‐valent vaccine will have on the hospitalization rate or mortality.

In contrast to the results for pneumococcal vaccination, studies of the benefits of influenza vaccination have shown clear and consistent reductions in mortality, respiratory illness, hospitalization, and pneumonia, especially among patients with comorbidities.6771 Cost effectiveness has been demonstrated for all populations,72, 73 and the reduction in mortality among high‐risk patients younger than age 65 has been estimated to be as high as 78%.68 Among the elderly, reduction in mortality of about 50% has been reported, along with 20%‐30% reductions in hospitalizations for pneumonia, influenza, cardiac disease, and stroke.70 Reduced incidence of pneumonia in vaccinated patients has even been documented among elderly patients without specific comorbidities.67 Annual revaccination has the most significant impact on mortality.74

The pneumococcal vaccine remains important in the effort to reduce the severity of and complications from invasive pneumococcal disease in the elderly, but the lack of significant benefits on hard end points such as mortality or hospitalizations makes it a less robust measure of quality pneumonia care. In contrast, influenza vaccination has a much larger impact on outcomes in the population at risk. Emphasis should be shifted from pneumococcal to influenza vaccine in pneumonia performance measures.

OXYGENATION ASSESSMENT

It seems intuitive that oxygenation assessment is important in the initial evaluation of patients with CAP, though there is not direct evidence to support this. The recommendation for oxygenation assessment in the published guidelines for CAP is by consensus.3335 Documented hypoxemia is associated with increased pneumonia‐related mortality,17, 75 and clinical judgment does not adequately predict hypoxemia.76 Though the assessment of oxygenation has been found to vary widely among practitioners,77 performance has remained consistent since the advent of monitoring and reporting of quality measures, with compliance rates of 99%.4, 7 Monitoring performance of this measure should continue, though high compliance rates limit its ability to discriminate among institutions.

SMOKING CESSATION COUNSELING

Counseling patients to stop smoking was found to be modestly (2%) but statistically significantly effective in promoting abstinence at 1 year.78 In its report on treating tobacco use, the U.S. Public Health Services recommended that all smokers receive hospital‐ and system‐based interventions at every visit.79 As part of the Pneumonia Patient Outcomes Research Team (PORT) study, smokers with pneumonia underwent a tobacco cessation interview. Though only 15% of these patients quit smoking, 93% of those who quit did so at the time they developed CAP.80 A retrospective study of patients with bacteremic pneumococcal pneumonia found tobacco exposure, including passive smoking, to be a strong independent risk factor for invasive disease.81 The most recent CAP guidelines from the Infectious Disease Society of America (IDSA) recommend smoking cessation counseling for all hospitalized patients who smoke.33 However, hospitals are not likely to have the impact that a more comprehensive, outpatient‐based smoking cessation program would. Without ongoing support, counseling, and pharmacotherapy, the effects of an intervention would be expected to be small.79 Though evidence of benefit is limited, smoking cessation interventions should be encouraged at all sites of care. Quality care merits this regardless of admitting diagnosis, but benefits specific to CAP outcomes have not yet been demonstrated.

CONCLUSIONS

The burden of illness caused by CAP mandates that clinicians strive to deliver the highest quality of care to afflicted patients. Critical evaluation of the strength of the evidence will continue to guide such endeavors, and changes in practice will follow as new information surfaces. Standards of care, as adopted by consensus groups such as the IDSA and American Thoracic Society, will continue to inform the practice of hospitalists.

How quality is defined for public reporting requires particularly careful assessment. The definition of quality should be based on evidence more rigorous than that ascribed to consensus guidelines. Within the profession, guidelines offer reasonable standards of care and delineate areas for further research and are invaluable tools for practicing clinicians. In the public arena, however, proclaiming practices as good or bad sets expectations of health care consumers not educated in the nuances of evaluating clinical evidence and can unfairly bias them against conscientious and effective providers whose standards reflect different interpretations of controversial issues. Regulatory agencies should publicly target interventions using only the most solid evidentiary foundation while internally striving to monitor the effects of different practice patterns and report measurable differences in outcomes revealed by careful investigation. Areas where controversy remains should be the primary targets of further research but should not be offered as benchmarks for public scrutiny until the medical community has settled on a position.

Furthermore, when evidence remains questionable, financial incentives should be linked to performance indicators with extreme caution. It would be counterproductive if health care organizations, driven to achieve optimal antibiotic timing to obtain payment updates from CMS, began to administer antibiotics prior to completing workups on all patients with respiratory complaints, as this would likely lead to antibiotic overuse. Similarly, institutions pushed to collect blood cultures before antibiotics are given may inappropriately delay administration in order to perform well on quality measures, resulting in potential harm to patients.

The measures of quality care for CAP for which the evidence on outcomes is the most convincing are antibiotic selection (mortality benefit, reduction in LOS) and influenza vaccination (mortality benefit, reduction in hospitalizations, reduction in respiratory illness). Antibiotic timing also shows a smaller but convincing reduction in mortality, though the advantages of receiving antibiotics within 4 hours instead of 8 hours are not clearly established for younger patients. These measures should be emphasized most heavily in the arena of public reporting and incentives for quality care, with additions and modifications guided by emerging evidence. Revision of the other measures to conform with current evidence would allow public reporting to more accurately reflect quality.

References
  1. Colice GL,Morley MA,Asche C,Birnbaum HG.Treatment costs of community‐acquired pneumonia in an employed population.Chest.2004;125:21402145.
  2. Kaplan V,Clermont G,Griffin MF, et al.Pneumonia: still the old man's friend?Arch Intern Med.2003;163:317323.
  3. Fry A SD,Holman R,Curns A,Anderson L.Trends in hospitalizations for pneumonia among persons aged 65 years or older in the United States, 1988‐2002.JAMA.2005;294:27122719.
  4. Williams SC,Schmaltz SP,Morton DJ,Koss RG,Loeb JM.Quality of care in U.S. hospitals as reflected by standardized measures, 2002‐2004.N Engl J Med.2005;353:255264.
  5. Performance Measurement: Core Measures. Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/index.htm. Accessed November 7, 2005.
  6. Medicare Quality Improvement Program Priorities: DRAFT, August2005.Centers for Medicare 353:265274.
  7. Medicare demonstration shows hospital quality of care improves with payments tied to quality.Centers for Medicare 278:20802084.
  8. Dedier J,Singer DE,Chang Y,Moore M,Atlas SJ.Processes of care, illness severity, and outcomes in the management of community‐acquired pneumonia at academic hospitals.Arch Intern Med.2001;161:20992104.
  9. Campbell SG,Marrie TJ,Anstey R,Dickinson G,Ackroyd‐Stolarz S.The contribution of blood cultures to the clinical management of adult patients admitted to the hospital with community‐acquired pneumonia: a prospective observational study.Chest.2003;123:11421150.
  10. Chalasani NP,Valdecanas MA,Gopal AK,McGowan JE,Jurado RL.Clinical utility of blood cultures in adult patients with community‐acquired pneumonia without defined underlying risks.Chest.1995;108:932936.
  11. Corbo J,Friedman B,Bijur P,Gallagher EJ.Limited usefulness of initial blood cultures in community acquired pneumonia.Emerg Med J.2004;21:446448.
  12. Waterer GW,Jennings SG,Wunderink RG.The impact of blood cultures on antibiotic therapy in pneumococcal pneumonia.Chest.1999;116:12781281.
  13. Waterer GW,Wunderink RG.The influence of the severity of community‐acquired pneumonia on the usefulness of blood cultures.Respir Med.2001;95(1):7882.
  14. Fine MJ,Auble TE,Yealy DM, et al.A prediction rule to identify low‐risk patients with community‐acquired pneumonia.N Engl J Med.1997;336:243250.
  15. Metersky ML,Ma A,Bratzler DW,Houck PM.Predicting bacteremia in patients with community‐acquired pneumonia.Am J Respir Crit Care Med.2004;169:342347.
  16. Theerthakarai R,El‐Halees W,Ismail M,Solis RA,Khan MA.Nonvalue of the initial microbiological studies in the management of nonsevere community‐acquired pneumonia.Chest.2001;119:181184.
  17. Battleman DS,Callahan M,Thaler HT.Rapid antibiotic delivery and appropriate antibiotic selection reduce length of hospital stay of patients with community‐acquired pneumonia: link between quality of care and resource utilization.Arch Intern Med.2002;162:682688.
  18. Silber SH,Garrett C,Singh R, et al.Early administration of antibiotics does not shorten time to clinical stability in patients with moderate‐to‐severe community‐acquired pneumonia.Chest.2003;124:17981804.
  19. Marrie TJ,Wu L.Factors influencing in‐hospital mortality in community‐acquired pneumonia: a prospective study of patients not initially admitted to the ICU.Chest.2005;127:12601270.
  20. Hospital Quality Measures:2004‐2007. Available at: http://www.cms.hhs.gov/quality/hospital/. Accessed November 17, 2005.
  21. National Hospital Quality Measures Specification Manual version 1.02.Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/aligned_manual.htm.
  22. Houck PM,Bratzler DW,Nsa W,Ma A,Bartlett JG.Timing of antibiotic administration and outcomes for Medicare patients hospitalized with community‐acquired pneumonia.Arch Intern Med.2004;164:637644.
  23. Metersky ML,Sweeney TA,Getzow MB,Siddiqui F,Nsa W,Bratzler DW.Antibiotic timing and diagnostic uncertainty in Medicare patients with pneumonia: is it reasonable to expect all patients to receive antibiotics within 4 hours?Chest.2006;130:1621.
  24. Houck PM,Bratzler DW.Administration of first hospital antibiotics for community‐acquired pneumonia: does timeliness affect outcomes?Curr Opin Infect Dis.2005;18(2):151156.
  25. Thompson D.The pneumonia controversy: hospitals grapple with 4 hour benchmark.Ann Emerg Med.2006;47:259261.
  26. Gonzales R,Bartlett JG,Besser RE, et al.Principles of appropriate antibiotic use for treatment of acute respiratory tract infections in adults: background, specific aims, and methods.Ann Intern Med.2001;134:479486.
  27. Garau J.The hidden impact of antibacterial resistance in respiratory tract infection. Clinical failures: the tip of the iceberg?Respir Med2001;95Suppl A:S511; discussion S26S27.
  28. Houck PM.Antibiotics and pneumonia: is timing everything or just a cause of more problems?Chest.2006;130:13.
  29. Gleason PP,Meehan TP,Fine JM,Galusha DH,Fine MJ.Associations between initial antimicrobial therapy and medical outcomes for hospitalized elderly patients with pneumonia.Arch Intern Med.1999;159:25622572.
  30. Mandell LA,Bartlett JG,Dowell SF,File TM,Musher DM,Whitney C.Update of practice guidelines for the management of community‐acquired pneumonia in immunocompetent adults.Clin Infect Dis.2003;37:14051433.
  31. Niederman MS,Mandell LA,Anzueto A, et al.Guidelines for the management of adults with community‐acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention.Am J Respir Crit Care Med.2001;163:17301754.
  32. Bartlett JG,Dowell SF,Mandell LA,File TM,Musher DM,Fine MJ.Practice guidelines for the management of community‐acquired pneumonia in adults.Infectious Diseases Society of America.Clin Infect Dis.2000;31:347382.
  33. Mortensen EM,Restrepo M,Anzueto A,Pugh J.Effects of guideline‐concordant antimicrobial therapy on mortality among patients with community‐acquired pneumonia.Am J Med.2004;117:726731.
  34. Flanders SA,Dudas V,Kerr K,McCulloch CE,Gonzales R.Effectiveness of ceftriaxone plus doxycycline in the treatment of patients hospitalized with community‐acquired pneumonia.J Hosp Med.2006;1:712.
  35. Waterer GW.Monotherapy versus combination antimicrobial therapy for pneumococcal pneumonia.Curr Opin Infect Dis.2005;18:157163.
  36. Weiss K,Tillotson GS.The controversy of combination vs monotherapy in the treatment of hospitalized community‐acquired pneumonia.Chest.2005;128:940946.
  37. Waterer GW,Somes GW,Wunderink RG.Monotherapy may be suboptimal for severe bacteremic pneumococcal pneumonia.Arch Intern Med.2001;161:18371842.
  38. Baddour LM,Yu VL,Klugman KP, et al.Combination antibiotic therapy lowers mortality among severely ill patients with pneumococcal bacteremia.Am J Respir Crit Care Med.2004;170:440444.
  39. Martinez JA,Horcajada JP,Almela M, et al.Addition of a macrolide to a beta‐lactam‐based empirical antibiotic regimen is associated with lower in‐hospital mortality for patients with bacteremic pneumococcal pneumonia.Clin Infect Dis.2003;36:389395.
  40. Weiss K,Low DE,Cortes L, et al.Clinical characteristics at initial presentation and impact of dual therapy on the outcome of bacteremic Streptococcus pneumoniae pneumonia in adults.Can Respir J.2004;11:589593.
  41. Brown RB,Iannini P,Gross P,Kunkel M.Impact of initial antibiotic choice on clinical outcomes in community‐acquired pneumonia: analysis of a hospital claims‐made database.Chest.2003;123:15031511.
  42. Shefet D,Robenshtok E,Paul M,Leibovici L.Empirical atypical coverage for inpatients with community‐acquired pneumonia: systematic review of randomized controlled trials.Arch Intern Med.2005;165:19922000.
  43. Shefet D,Robenshtock E,Paul M,Leibovici L.Empiric antibiotic coverage of atypical pathogens for community acquired pneumonia in hospitalized adults.Cochrane Database Syst. Rev.2005:CD004418.
  44. Mills GD,Oehley MR,Arrol B.Effectiveness of beta lactam antibiotics compared with antibiotics active against atypical pathogens in non‐severe community acquired pneumonia: meta‐analysis.Br Med J.2005;330:456.
  45. Lin E,Stanek RJ,Mufson MA.Lack of synergy of erythromycin combined with penicillin or cefotaxime against Streptococcus pneumoniae in vitro.Antimicrob Agents Chemother.2003;47:11511153.
  46. Johansen HK,Jensen TG,Dessau RB,Lundgren B,Frimodt‐Moller N.Antagonism between penicillin and erythromycin against Streptococcus pneumoniae in vitro and in vivo.J Antimicrob Chemother.2000;46:973980.
  47. Tamaoki J.The effects of macrolides on inflammatory cells.Chest.2004;125(2 Suppl):41S50S; quiz 1S.
  48. Ruiz M,Ewig S,Torres A, et al.Severe community‐acquired pneumonia. Risk factors and follow‐up epidemiology.Am J Respir Crit Care Med.1999;160:923929.
  49. Ewig S,Ruiz M,Mensa J, et al.Severe community‐acquired pneumonia. Assessment of severity criteria.Am J Respir Crit Care Med.1998;158:11021108.
  50. Willis BC,Ndiaye SM,Hopkins DP,Shefer A.Improving influenza, pneumococcal polysaccharide, and hepatitis B vaccination coverage among adults aged <65 years at high risk: a report on recommendations of the Task Force on Community Preventive Services.MMWR Recomm Rep.2005;54(RR‐5):111.
  51. Conaty S,Watson L,Dinnes J,Waugh N.The effectiveness of pneumococcal polysaccharide vaccines in adults: a systematic review of observational studies and comparison with results from randomised controlled trials.Vaccine.2004;22:32143224.
  52. Watson L,Wilson BJ,Waugh N.Pneumococcal polysaccharide vaccine: a systematic review of clinical effectiveness in adults.Vaccine.2002;20:21662173.
  53. Jackson LA,Neuzil KM,Yu O, et al.Effectiveness of pneumococcal polysaccharide vaccine in older adults.N Engl J Med.2003;348:17471755.
  54. Butler JC,Breiman RF,Campbell JF,Lipman HB,Broome CV,Facklam RR.Pneumococcal polysaccharide vaccine efficacy. An evaluation of current recommendations.JAMA.1993;270:18261831.
  55. Balakrishnan I,Crook P,Morris R,Gillespie SH.Early predictors of mortality in pneumococcal bacteraemia.J Infect.2000;40:256261.
  56. Afessa B,Greaves WL,Frederick WR.Pneumococcal bacteremia in adults: a 14‐year experience in an inner‐city university hospital.Clin Infect Dis.1995;21:345351.
  57. Laurichesse H,Grimaud O,Waight P,Johnson AP,George RC,Miller E.Pneumococcal bacteraemia and meningitis in England and Wales, 1993 to 1995.Commun Dis Public Health.1998;1(1):2227.
  58. Kramer MR,Rudensky B,Hadas‐Halperin I,Isacsohn M,Melzer E.Pneumococcal bacteremia—no change in mortality in 30 years: analysis of 104 cases and review of the literature.Isr J Med Sci.1987;23:174180.
  59. Dear K,Holden J,Andrews R,Tatham D.Vaccines for preventing pneumococcal infection in adults.Cochrane Database Syst Rev.2003:CD000422.
  60. Nichol KL,Baken L,Wuorenma J,Nelson A.The health and economic benefits associated with pneumococcal vaccination of elderly persons with chronic lung disease.Arch Intern Med.1999;159:24372442.
  61. Lexau CA,Lynfield R,Danila R, et al.Changing epidemiology of invasive pneumococcal disease among older adults in the era of pediatric pneumococcal conjugate vaccine.JAMA.2005;294:20432051.
  62. Whitney CG,Farley MM,Hadler J, et al.Decline in invasive pneumococcal disease after the introduction of protein‐polysaccharide conjugate vaccine.N Engl J Med.2003;348:17371746.
  63. Kyaw MH,Lynfield R,Schaffner W, et al.Effect of introduction of the pneumococcal conjugate vaccine on drug‐resistant Streptococcus pneumoniae.N Engl J Med.2006;354:14551463.
  64. Voordouw BC,van der Linden PD,Simonian S,van der Lei J,Sturkenboom MC,Stricker BH.Influenza vaccination in community‐dwelling elderly: impact on mortality and influenza‐associated morbidity.Arch Intern Med.2003;163:10891094.
  65. Hak E,Buskens E,van Essen GA, et al.Clinical effectiveness of influenza vaccination in persons younger than 65 years with high‐risk medical conditions: the PRISMA study.Arch Intern Med.2005;165:274280.
  66. Hak E,Nordin J,Wei F, et al.Influence of high‐risk medical conditions on the effectiveness of influenza vaccination among elderly members of 3 large managed‐care organizations.Clin Infect Dis.2002;35:370377.
  67. Nichol KL,Nordin J,Mullooly J,Lask R,Fillbrandt K,Iwane M.Influenza vaccination and reduction in hospitalizations for cardiac disease and stroke among the elderly.N Engl J Med.2003;348:13221332.
  68. Wongsurakiat P,Maranetra KN,Wasi C,Kositanont U,Dejsomritrutai W,Charoenratanakul S.Acute respiratory illness in patients with COPD and the effectiveness of influenza vaccination: a randomized controlled study.Chest.2004;125:20112020.
  69. Lee PY,Matchar DB,Clements DA,Huber J,Hamilton JD,Peterson ED.Economic analysis of influenza vaccination and antiviral treatment for healthy working adults.Ann Intern Med.2002;137:225331.
  70. Gross PA,Hermogenes AW,Sacks HS,Lau J,Levandowski RA.The efficacy of influenza vaccine in elderly persons. A meta‐analysis and review of the literature.Ann Intern Med.1995;123:518527.
  71. Voordouw AC,Sturkenboom MC,Dieleman JP, et al.Annual revaccination against influenza and mortality risk in community‐dwelling elderly persons.JAMA.2004;292:20892095.
  72. Mortensen EM,Coley CM,Singer DE, et al.Causes of death for patients with community‐acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team cohort study.Arch Intern Med.2002;162:10591064.
  73. Maneker AJ,Petrack EM,Krug SE.Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department.Ann Emerg Med.1995;25(1):3640.
  74. Levin KP,Hanusa BH,Rotondi A, et al.Arterial blood gas and pulse oximetry in initial management of patients with community‐acquired pneumonia.J Gen Intern Med.2001;16:590598.
  75. Law M,Tang JL.An analysis of the effectiveness of interventions intended to help people stop smoking.Arch Intern Med.1995;155:19331941.
  76. A clinical practice guideline for treating tobacco use and dependence: A US Public Health Service report.The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium Representatives.JAMA.2000;283:32443254.
  77. Rhew DC.Quality indicators for the management of pneumonia in vulnerable elders.Ann Intern Med.2001;135:736743.
  78. Nuorti JP,Butler JC,Farley MM, et al.Cigarette smoking and invasive pneumococcal disease.Active Bacterial Core Surveillance Team.N Engl J Med.2000;342:681689.
References
  1. Colice GL,Morley MA,Asche C,Birnbaum HG.Treatment costs of community‐acquired pneumonia in an employed population.Chest.2004;125:21402145.
  2. Kaplan V,Clermont G,Griffin MF, et al.Pneumonia: still the old man's friend?Arch Intern Med.2003;163:317323.
  3. Fry A SD,Holman R,Curns A,Anderson L.Trends in hospitalizations for pneumonia among persons aged 65 years or older in the United States, 1988‐2002.JAMA.2005;294:27122719.
  4. Williams SC,Schmaltz SP,Morton DJ,Koss RG,Loeb JM.Quality of care in U.S. hospitals as reflected by standardized measures, 2002‐2004.N Engl J Med.2005;353:255264.
  5. Performance Measurement: Core Measures. Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/index.htm. Accessed November 7, 2005.
  6. Medicare Quality Improvement Program Priorities: DRAFT, August2005.Centers for Medicare 353:265274.
  7. Medicare demonstration shows hospital quality of care improves with payments tied to quality.Centers for Medicare 278:20802084.
  8. Dedier J,Singer DE,Chang Y,Moore M,Atlas SJ.Processes of care, illness severity, and outcomes in the management of community‐acquired pneumonia at academic hospitals.Arch Intern Med.2001;161:20992104.
  9. Campbell SG,Marrie TJ,Anstey R,Dickinson G,Ackroyd‐Stolarz S.The contribution of blood cultures to the clinical management of adult patients admitted to the hospital with community‐acquired pneumonia: a prospective observational study.Chest.2003;123:11421150.
  10. Chalasani NP,Valdecanas MA,Gopal AK,McGowan JE,Jurado RL.Clinical utility of blood cultures in adult patients with community‐acquired pneumonia without defined underlying risks.Chest.1995;108:932936.
  11. Corbo J,Friedman B,Bijur P,Gallagher EJ.Limited usefulness of initial blood cultures in community acquired pneumonia.Emerg Med J.2004;21:446448.
  12. Waterer GW,Jennings SG,Wunderink RG.The impact of blood cultures on antibiotic therapy in pneumococcal pneumonia.Chest.1999;116:12781281.
  13. Waterer GW,Wunderink RG.The influence of the severity of community‐acquired pneumonia on the usefulness of blood cultures.Respir Med.2001;95(1):7882.
  14. Fine MJ,Auble TE,Yealy DM, et al.A prediction rule to identify low‐risk patients with community‐acquired pneumonia.N Engl J Med.1997;336:243250.
  15. Metersky ML,Ma A,Bratzler DW,Houck PM.Predicting bacteremia in patients with community‐acquired pneumonia.Am J Respir Crit Care Med.2004;169:342347.
  16. Theerthakarai R,El‐Halees W,Ismail M,Solis RA,Khan MA.Nonvalue of the initial microbiological studies in the management of nonsevere community‐acquired pneumonia.Chest.2001;119:181184.
  17. Battleman DS,Callahan M,Thaler HT.Rapid antibiotic delivery and appropriate antibiotic selection reduce length of hospital stay of patients with community‐acquired pneumonia: link between quality of care and resource utilization.Arch Intern Med.2002;162:682688.
  18. Silber SH,Garrett C,Singh R, et al.Early administration of antibiotics does not shorten time to clinical stability in patients with moderate‐to‐severe community‐acquired pneumonia.Chest.2003;124:17981804.
  19. Marrie TJ,Wu L.Factors influencing in‐hospital mortality in community‐acquired pneumonia: a prospective study of patients not initially admitted to the ICU.Chest.2005;127:12601270.
  20. Hospital Quality Measures:2004‐2007. Available at: http://www.cms.hhs.gov/quality/hospital/. Accessed November 17, 2005.
  21. National Hospital Quality Measures Specification Manual version 1.02.Joint Commission on Accreditation of Healthcare Organizations,2005. Available at: http://www.jcaho.org/pms/core+measures/aligned_manual.htm.
  22. Houck PM,Bratzler DW,Nsa W,Ma A,Bartlett JG.Timing of antibiotic administration and outcomes for Medicare patients hospitalized with community‐acquired pneumonia.Arch Intern Med.2004;164:637644.
  23. Metersky ML,Sweeney TA,Getzow MB,Siddiqui F,Nsa W,Bratzler DW.Antibiotic timing and diagnostic uncertainty in Medicare patients with pneumonia: is it reasonable to expect all patients to receive antibiotics within 4 hours?Chest.2006;130:1621.
  24. Houck PM,Bratzler DW.Administration of first hospital antibiotics for community‐acquired pneumonia: does timeliness affect outcomes?Curr Opin Infect Dis.2005;18(2):151156.
  25. Thompson D.The pneumonia controversy: hospitals grapple with 4 hour benchmark.Ann Emerg Med.2006;47:259261.
  26. Gonzales R,Bartlett JG,Besser RE, et al.Principles of appropriate antibiotic use for treatment of acute respiratory tract infections in adults: background, specific aims, and methods.Ann Intern Med.2001;134:479486.
  27. Garau J.The hidden impact of antibacterial resistance in respiratory tract infection. Clinical failures: the tip of the iceberg?Respir Med2001;95Suppl A:S511; discussion S26S27.
  28. Houck PM.Antibiotics and pneumonia: is timing everything or just a cause of more problems?Chest.2006;130:13.
  29. Gleason PP,Meehan TP,Fine JM,Galusha DH,Fine MJ.Associations between initial antimicrobial therapy and medical outcomes for hospitalized elderly patients with pneumonia.Arch Intern Med.1999;159:25622572.
  30. Mandell LA,Bartlett JG,Dowell SF,File TM,Musher DM,Whitney C.Update of practice guidelines for the management of community‐acquired pneumonia in immunocompetent adults.Clin Infect Dis.2003;37:14051433.
  31. Niederman MS,Mandell LA,Anzueto A, et al.Guidelines for the management of adults with community‐acquired pneumonia. Diagnosis, assessment of severity, antimicrobial therapy, and prevention.Am J Respir Crit Care Med.2001;163:17301754.
  32. Bartlett JG,Dowell SF,Mandell LA,File TM,Musher DM,Fine MJ.Practice guidelines for the management of community‐acquired pneumonia in adults.Infectious Diseases Society of America.Clin Infect Dis.2000;31:347382.
  33. Mortensen EM,Restrepo M,Anzueto A,Pugh J.Effects of guideline‐concordant antimicrobial therapy on mortality among patients with community‐acquired pneumonia.Am J Med.2004;117:726731.
  34. Flanders SA,Dudas V,Kerr K,McCulloch CE,Gonzales R.Effectiveness of ceftriaxone plus doxycycline in the treatment of patients hospitalized with community‐acquired pneumonia.J Hosp Med.2006;1:712.
  35. Waterer GW.Monotherapy versus combination antimicrobial therapy for pneumococcal pneumonia.Curr Opin Infect Dis.2005;18:157163.
  36. Weiss K,Tillotson GS.The controversy of combination vs monotherapy in the treatment of hospitalized community‐acquired pneumonia.Chest.2005;128:940946.
  37. Waterer GW,Somes GW,Wunderink RG.Monotherapy may be suboptimal for severe bacteremic pneumococcal pneumonia.Arch Intern Med.2001;161:18371842.
  38. Baddour LM,Yu VL,Klugman KP, et al.Combination antibiotic therapy lowers mortality among severely ill patients with pneumococcal bacteremia.Am J Respir Crit Care Med.2004;170:440444.
  39. Martinez JA,Horcajada JP,Almela M, et al.Addition of a macrolide to a beta‐lactam‐based empirical antibiotic regimen is associated with lower in‐hospital mortality for patients with bacteremic pneumococcal pneumonia.Clin Infect Dis.2003;36:389395.
  40. Weiss K,Low DE,Cortes L, et al.Clinical characteristics at initial presentation and impact of dual therapy on the outcome of bacteremic Streptococcus pneumoniae pneumonia in adults.Can Respir J.2004;11:589593.
  41. Brown RB,Iannini P,Gross P,Kunkel M.Impact of initial antibiotic choice on clinical outcomes in community‐acquired pneumonia: analysis of a hospital claims‐made database.Chest.2003;123:15031511.
  42. Shefet D,Robenshtok E,Paul M,Leibovici L.Empirical atypical coverage for inpatients with community‐acquired pneumonia: systematic review of randomized controlled trials.Arch Intern Med.2005;165:19922000.
  43. Shefet D,Robenshtock E,Paul M,Leibovici L.Empiric antibiotic coverage of atypical pathogens for community acquired pneumonia in hospitalized adults.Cochrane Database Syst. Rev.2005:CD004418.
  44. Mills GD,Oehley MR,Arrol B.Effectiveness of beta lactam antibiotics compared with antibiotics active against atypical pathogens in non‐severe community acquired pneumonia: meta‐analysis.Br Med J.2005;330:456.
  45. Lin E,Stanek RJ,Mufson MA.Lack of synergy of erythromycin combined with penicillin or cefotaxime against Streptococcus pneumoniae in vitro.Antimicrob Agents Chemother.2003;47:11511153.
  46. Johansen HK,Jensen TG,Dessau RB,Lundgren B,Frimodt‐Moller N.Antagonism between penicillin and erythromycin against Streptococcus pneumoniae in vitro and in vivo.J Antimicrob Chemother.2000;46:973980.
  47. Tamaoki J.The effects of macrolides on inflammatory cells.Chest.2004;125(2 Suppl):41S50S; quiz 1S.
  48. Ruiz M,Ewig S,Torres A, et al.Severe community‐acquired pneumonia. Risk factors and follow‐up epidemiology.Am J Respir Crit Care Med.1999;160:923929.
  49. Ewig S,Ruiz M,Mensa J, et al.Severe community‐acquired pneumonia. Assessment of severity criteria.Am J Respir Crit Care Med.1998;158:11021108.
  50. Willis BC,Ndiaye SM,Hopkins DP,Shefer A.Improving influenza, pneumococcal polysaccharide, and hepatitis B vaccination coverage among adults aged <65 years at high risk: a report on recommendations of the Task Force on Community Preventive Services.MMWR Recomm Rep.2005;54(RR‐5):111.
  51. Conaty S,Watson L,Dinnes J,Waugh N.The effectiveness of pneumococcal polysaccharide vaccines in adults: a systematic review of observational studies and comparison with results from randomised controlled trials.Vaccine.2004;22:32143224.
  52. Watson L,Wilson BJ,Waugh N.Pneumococcal polysaccharide vaccine: a systematic review of clinical effectiveness in adults.Vaccine.2002;20:21662173.
  53. Jackson LA,Neuzil KM,Yu O, et al.Effectiveness of pneumococcal polysaccharide vaccine in older adults.N Engl J Med.2003;348:17471755.
  54. Butler JC,Breiman RF,Campbell JF,Lipman HB,Broome CV,Facklam RR.Pneumococcal polysaccharide vaccine efficacy. An evaluation of current recommendations.JAMA.1993;270:18261831.
  55. Balakrishnan I,Crook P,Morris R,Gillespie SH.Early predictors of mortality in pneumococcal bacteraemia.J Infect.2000;40:256261.
  56. Afessa B,Greaves WL,Frederick WR.Pneumococcal bacteremia in adults: a 14‐year experience in an inner‐city university hospital.Clin Infect Dis.1995;21:345351.
  57. Laurichesse H,Grimaud O,Waight P,Johnson AP,George RC,Miller E.Pneumococcal bacteraemia and meningitis in England and Wales, 1993 to 1995.Commun Dis Public Health.1998;1(1):2227.
  58. Kramer MR,Rudensky B,Hadas‐Halperin I,Isacsohn M,Melzer E.Pneumococcal bacteremia—no change in mortality in 30 years: analysis of 104 cases and review of the literature.Isr J Med Sci.1987;23:174180.
  59. Dear K,Holden J,Andrews R,Tatham D.Vaccines for preventing pneumococcal infection in adults.Cochrane Database Syst Rev.2003:CD000422.
  60. Nichol KL,Baken L,Wuorenma J,Nelson A.The health and economic benefits associated with pneumococcal vaccination of elderly persons with chronic lung disease.Arch Intern Med.1999;159:24372442.
  61. Lexau CA,Lynfield R,Danila R, et al.Changing epidemiology of invasive pneumococcal disease among older adults in the era of pediatric pneumococcal conjugate vaccine.JAMA.2005;294:20432051.
  62. Whitney CG,Farley MM,Hadler J, et al.Decline in invasive pneumococcal disease after the introduction of protein‐polysaccharide conjugate vaccine.N Engl J Med.2003;348:17371746.
  63. Kyaw MH,Lynfield R,Schaffner W, et al.Effect of introduction of the pneumococcal conjugate vaccine on drug‐resistant Streptococcus pneumoniae.N Engl J Med.2006;354:14551463.
  64. Voordouw BC,van der Linden PD,Simonian S,van der Lei J,Sturkenboom MC,Stricker BH.Influenza vaccination in community‐dwelling elderly: impact on mortality and influenza‐associated morbidity.Arch Intern Med.2003;163:10891094.
  65. Hak E,Buskens E,van Essen GA, et al.Clinical effectiveness of influenza vaccination in persons younger than 65 years with high‐risk medical conditions: the PRISMA study.Arch Intern Med.2005;165:274280.
  66. Hak E,Nordin J,Wei F, et al.Influence of high‐risk medical conditions on the effectiveness of influenza vaccination among elderly members of 3 large managed‐care organizations.Clin Infect Dis.2002;35:370377.
  67. Nichol KL,Nordin J,Mullooly J,Lask R,Fillbrandt K,Iwane M.Influenza vaccination and reduction in hospitalizations for cardiac disease and stroke among the elderly.N Engl J Med.2003;348:13221332.
  68. Wongsurakiat P,Maranetra KN,Wasi C,Kositanont U,Dejsomritrutai W,Charoenratanakul S.Acute respiratory illness in patients with COPD and the effectiveness of influenza vaccination: a randomized controlled study.Chest.2004;125:20112020.
  69. Lee PY,Matchar DB,Clements DA,Huber J,Hamilton JD,Peterson ED.Economic analysis of influenza vaccination and antiviral treatment for healthy working adults.Ann Intern Med.2002;137:225331.
  70. Gross PA,Hermogenes AW,Sacks HS,Lau J,Levandowski RA.The efficacy of influenza vaccine in elderly persons. A meta‐analysis and review of the literature.Ann Intern Med.1995;123:518527.
  71. Voordouw AC,Sturkenboom MC,Dieleman JP, et al.Annual revaccination against influenza and mortality risk in community‐dwelling elderly persons.JAMA.2004;292:20892095.
  72. Mortensen EM,Coley CM,Singer DE, et al.Causes of death for patients with community‐acquired pneumonia: results from the Pneumonia Patient Outcomes Research Team cohort study.Arch Intern Med.2002;162:10591064.
  73. Maneker AJ,Petrack EM,Krug SE.Contribution of routine pulse oximetry to evaluation and management of patients with respiratory illness in a pediatric emergency department.Ann Emerg Med.1995;25(1):3640.
  74. Levin KP,Hanusa BH,Rotondi A, et al.Arterial blood gas and pulse oximetry in initial management of patients with community‐acquired pneumonia.J Gen Intern Med.2001;16:590598.
  75. Law M,Tang JL.An analysis of the effectiveness of interventions intended to help people stop smoking.Arch Intern Med.1995;155:19331941.
  76. A clinical practice guideline for treating tobacco use and dependence: A US Public Health Service report.The Tobacco Use and Dependence Clinical Practice Guideline Panel, Staff, and Consortium Representatives.JAMA.2000;283:32443254.
  77. Rhew DC.Quality indicators for the management of pneumonia in vulnerable elders.Ann Intern Med.2001;135:736743.
  78. Nuorti JP,Butler JC,Farley MM, et al.Cigarette smoking and invasive pneumococcal disease.Active Bacterial Core Surveillance Team.N Engl J Med.2000;342:681689.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
344-353
Page Number
344-353
Article Type
Display Headline
Community‐acquired pneumonia: Defining quality care
Display Headline
Community‐acquired pneumonia: Defining quality care
Legacy Keywords
community‐acquired and nosocomial pneumonia, quality improvement, care standardization
Legacy Keywords
community‐acquired and nosocomial pneumonia, quality improvement, care standardization
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
Associate Clinical Professor, Division of Hospital Medicine, Department of Medicine, University of California, San Diego, School of Medicine, 200 West Arbor Dr., San Diego, CA 92103‐8485; Fax: (619) 543‐8255
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Effect of Educational Intervention on Intern Confidence

Article Type
Changed
Sun, 05/28/2017 - 22:45
Display Headline
What effect does an educational intervention have on interns' confidence and knowledge regarding acute dyspnea management?. A randomized controlled trial

Cross‐cover is defined as an on‐call physician managing acute problems such as chest pain, dyspnea, and hypoxemia for patients primarily cared for by another physician. Cross‐cover problems are commonly encountered with hospitalized patients, and inappropriate evaluation and management can result in misdiagnosis. Residents in many internal medicine residency programs receive only informal instruction about how to manage cross‐cover problems, usually from senior medical residents. Unfortunately, instruction is often provided while a patient is experiencing a problem, a frequent occurrence in the chaotic circumstances of a stressful learning environment. Furthermore, the knowledge base, experience, and teaching skills of senior residents vary substantially, and typically senior residents receive no formal instruction to guide them in how or what to teach more junior residents. If formal instruction is provided to residents, it is typically through often poorly attended didactic lectures that have been shown to be an ineffective forum for acquiring skills or changing physician behavior.15

Although previous studies did find that educational interventions can improve confidence and increase knowledge about various aspects of residency training, many of these studies were not randomized,68 or they involved complex interventions requiring a significant amount of resident and teaching staff time.911 The few randomized studies that used simple educational interventions focused on outpatient education, but most of a resident's time is spent in an inpatient setting.1213

Therefore, we designed a simple, randomized educational intervention consisting of 2 formal small‐group, case‐based discussion sessions addressing 1 cross‐cover situation: a hospitalized patient with acute dyspnea. We hypothesized that the addition of small‐group sessions would improve intern knowledge about and confidence in managing acute dyspnea above that gained from a combination of informal education and formal but lecture‐based education.

METHODS

Thirty‐eight internal medicine residents in their first year of postgraduate training (interns) at the University of Michigan were approached to participate in the study. Twenty‐six interns signed informed consent forms and were randomized using a random number generator to receive either the standard education (the control group) or the standard education plus the educational intervention (the intervention group). The standard education was informal teaching by senior medical residents on the wards and a 1‐hour lecture on Approach to the Patient with Acute Dyspnea, taught by an attending physician from the Department of Pulmonary and Critical Care Medicine. The educational intervention included the standard education as well as 2 small‐group, case‐based interactive sessions on acute dyspnea management. Both sessions were developed and taught by the first author (T.M.R.), a third‐year resident in internal medicine. A senior resident taught the sessions to try to make the information more relevant and practical and to make asking questions less intimidating. The first session, which lasted 50 minutes, discussed cases of bronchospasm, pulmonary edema, and pulmonary embolism as causes of acute dyspnea. It addressed several concepts: knowing when and how quickly to evaluate a dyspneic patient, formulating a differential diagnosis, appropriately evaluating acute dyspnea, providing empiric therapy, and recognizing indications for intubation. The second small‐group session occurred approximately 1 month after the first session and lasted 30 minutes. In this session key concepts learned during the first session were reviewed, and a case of ventricular tachycardia presenting as acute dyspnea was discussed. In an effort to increase attendance, free food and drink were provided at each session, and participants were sent reminders via e‐mail and the paging system prior to each session.

All study participants completed pre‐ and postintervention surveys that assessed their knowledge of acute dyspnea management and their confidence in managing patients with this condition. The pretests were conducted just before the first small‐group session was held. The post‐tests were conducted 4 months later. Knowledge was assessed by the score on the 45‐point test, which contained both open‐ and closed‐ended questions derived from 10 case‐based items. The number of points that a question was worth varied depending on how many elements made up a correct answer. For example, one question asked, What tests (if any) do you plan to order immediately after you examine the patient? As 3 tests should have been obtained (EKG, CXR, and ABG), this item had a maximum score of 3 points. Confidence was assessed by averaging 17 items scored on a 5‐point Likert scale (from strongly agree to strongly disagree). The items measured the physician's confidence in managing various aspects of the dyspneic patient (eg, confidence in knowing when to intubate a patient, when to obtain an ABG/CXR/EKG, and when to transfer a patient to the ICU). Data were analyzed using repeated‐measures analysis of variance. Primary analysis was based on the intention‐to‐treat principle, with alpha set to .05 (2‐sided). A secondary, per‐protocol analysis was also performed. In this analysis, study participants who attended both small‐group sessions (ie, completed the entire intervention) were compared with the control group. The protocol was approved by the institutional review board at the University of Michigan Health System.

RESULTS

All participants completed the study. Overall, only 3 of the 26 interns attended the lecture on Approach to the Patient with Acute Dyspnea. Fourteen of the 16 interns assigned to the intervention group attended 1 of the 2 small‐group sessions (11 attended the first session, and 10 attended the second session). Seven interns attended both sessions. The study period was 4 months. Both the intervention and control groups reported managing a similar number of patients with acute dyspnea, both prior to the study (mean of 5.9 in the intervention group and 7.4 in the control group, P = .51) and at the end of study (mean 10.6 in the intervention group and 10.2 in the control group, P = .91). There was no significant difference in the total number of completed inpatient months (mean of 4.9 in the intervention group and 4.7 in the control group, P =. 32) or in the number of inpatient months completed prior to the start of the study (mean of 2 in the intervention group and 2.4 in the control group, P = .15).

Confidence

Subjects in both the intervention and control groups showed increased confidence over time. The mean score of the intervention group increased from 3.77 to 4.57 (a 21.2% increase) and that of the control group increased from 3.74 to 4.28 (a 14.4% increase). Although the trend over time was highly significant for both groups (P < .001), the effect of the intervention was not significant (P = .19). However, the power to detect a difference between the groups was low (0.25). In the per‐protocol analysis, there was no significant difference between the groups (P = .26; see Fig. 1).

Figure 1
Change in confidence pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

Knowledge

In the primary analysis, results for knowledge were similar to those obtained for the confidence outcome. In the intervention group, the mean score increased from 35.6 to 38.3 (a 7.6% increase); in the control group, the mean increased from 36.2 to 38.2 (a 5.5% increase). Scores ranged from 31 to 42. Again, the trend for both groups was significant (P < .01), but the effect of the intervention was not significant (P = .65). The power to detect a difference between groups was again low (0.07). In the per‐protocol analysis a trend toward significance was seen, with mean scores increasing from 34.6 to 40.0, a 15.6% increase (P = .067; see Fig. 2).

Figure 2
Change in knowledge pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

DISCUSSION

Our randomized controlled trial found that intern confidence and knowledge about acute dyspnea management both increased significantly over time; however, no significant differences between the intervention and control groups were observed. The complete intervention was not administered to the vast majority of those in the intervention group, however, likely skewing results toward the null. As suggested by the per‐protocol analysis, there was a trend toward a significant increase in the knowledge of the interns who had received the entire intervention. This is similar to results found in a randomized study by Schroy et al., which demonstrated a significant increase in resident knowledge of colorectal cancer screening after an educational intervention that used an interactive, case‐based seminar.13

Our study had several strengths. First, we employed the most robust design to detect efficacy, a randomized controlled study design. Second, we had complete follow‐up because all participants finished the study. Finally, our intervention is easily reproducible.

Our findings should also be considered within the context of several limitations. Despite the use of a random number generator, the control and intervention groups were unequal in number, which may have affected the results, particularly with such a small sample size.

Second, the intervention did not occur until 3 months after the start of each participant's internship. The intention was to implement the intervention at the start of internship, but institutional review board approval did not occur for an additional 3 months. This late timing might have been unfortunate because interns may already have had an established management plan for acute dyspnea, making their behavior more difficult to alter, even with additional education.

Third, because we were unaware of available test instruments to assess resident knowledge of acute dyspnea in the hospitalized patient, we needed to create our own. Unfortunately, the instrument yielded only a small variance in test scores, which may have made it difficult to detect an effect on scores if present.

Fourth, attendance at each session was suboptimal, and thus the complete intervention was not administered to the vast majority of those in the intervention group. Because the first small‐group session was the main teaching session, interns who only attended the second session were exposed to just one case discussion and only a review, rather than a full formal discussion, of the material presented during the first session. Therefore, it is not known if the intervention really had no effect or if no differences were detected simply because the complete intervention was not received. The trend toward significance observed in the per‐protocol analysis suggests that compliance with the intervention may be the key to improving knowledge.

Given the small differences observed in this study, future interventions ideally should use a more sensitive testing instrument, a larger sample, and a more powerful intervention that occurs early in training. Future efforts should also be designed to improve attendance at educational interventions. In the setting of reduced resident work hours and increased demands on resident time, this will prove to be a true challenge for all educators and residency programs.

References
  1. Carney PA,Dietrich AJ,Freeman DH,Mott LA.A standardized‐patient assessment of a continuing medical education program to improve physicians' cancer‐control clinical skills.Acad Med.1995;70(1):5258.
  2. Roche AM,Eccleston P,Sanson‐Fisher R.Teaching smoking cessation skills to senior medical students: a block‐randomized controlled trial of four different approaches.Prev Med.1996;25:251258.
  3. Davis D,O'Brien MA,Freemantle N,Wolf FM,Mazmanian P,Taylor‐Vaisey A.Impact of formal continuing medical education: Do conferences, workshops, rounds, and other traditional continuing education activities change physician behavior or health care outcomes?JAMA.1999;282:867874.
  4. Smits PB,de Buisonje CD,Verbeek JH,van Dijk FJ,Metz JC,ten Cate OJ.Problem‐based learning versus lecture‐based learning in postgraduate medical education.Scand J Work Environ Health.2003;29:280287.
  5. Herbert CP,Wright JM,Maclure M,Wakefield J,Dormuth C,Brett‐MacLean P,Legare J,Premi J.Better Prescribing Project: A randomized controlled trial of the impact of case‐based educational modules and personal prescribing feedback on prescribing for hypertension in primary care.Family Pract.2004;21:575581.
  6. Hillenbrand KM,Larsen PG.Effect of an educational intervention about breastfeeding on the knowledge, confidence, and behaviors of pediatric resident physicians.Pediatrics.2002;110(5):e59.
  7. Learman LA,Gerrity MS,Field DR,van Blaricom A,Romm J,Choe J.Effects of a depression education program on residents' knowledge, attitudes, and clinical skills.Obstet Gynecol.2003;101(1):167174.
  8. Meier AH,Henry J,Marine R,Murray WB.Implementation of a web‐ and simulation‐based curriculum to ease the transition from medical school to surgical internship.Am J Surg.2005;190(1):137140.
  9. Smith RC,Lyles JS,Mettler J, et al.The effectiveness of intensive training for residents in interviewing.Ann Intern Med.1998;128(2):118126.
  10. Murdoch Eaton D,Cottrell D.Structured teaching methods enhance skill acquisition but not problem‐solving abilities: an evaluation of the “silent run through.”Med Educ.1999;33:019023.
  11. Abraham A,Cheng T,Wright J,Addlestone I,Huang Z,Greenberg L.An educational intervention to improve physician violence screening skills.Pediatrics.2001;107(5):e68.
  12. D'Onofrio G,Nadel ES,Degutis LC,Sullivan LM,Casper K,Bernstein E,Samet JH.Improving emergency medicine residents' approach to patients with alcohol problems: a controlled educational trial.Ann Emerg Med.2002;40(1):5062.
  13. Schroy PC,Glick JT,Geller AC,Jackson A,Heeren T,Prout M.A novel educational strategy to enhance internal medicine residents' familial colorectal cancer knowledge and risk assessment skills.Am J Gastroenterol.2005;100:677684.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
339-343
Legacy Keywords
medical education, dyspnea, diagnostic error, respiratory tract diseases
Sections
Article PDF
Article PDF

Cross‐cover is defined as an on‐call physician managing acute problems such as chest pain, dyspnea, and hypoxemia for patients primarily cared for by another physician. Cross‐cover problems are commonly encountered with hospitalized patients, and inappropriate evaluation and management can result in misdiagnosis. Residents in many internal medicine residency programs receive only informal instruction about how to manage cross‐cover problems, usually from senior medical residents. Unfortunately, instruction is often provided while a patient is experiencing a problem, a frequent occurrence in the chaotic circumstances of a stressful learning environment. Furthermore, the knowledge base, experience, and teaching skills of senior residents vary substantially, and typically senior residents receive no formal instruction to guide them in how or what to teach more junior residents. If formal instruction is provided to residents, it is typically through often poorly attended didactic lectures that have been shown to be an ineffective forum for acquiring skills or changing physician behavior.15

Although previous studies did find that educational interventions can improve confidence and increase knowledge about various aspects of residency training, many of these studies were not randomized,68 or they involved complex interventions requiring a significant amount of resident and teaching staff time.911 The few randomized studies that used simple educational interventions focused on outpatient education, but most of a resident's time is spent in an inpatient setting.1213

Therefore, we designed a simple, randomized educational intervention consisting of 2 formal small‐group, case‐based discussion sessions addressing 1 cross‐cover situation: a hospitalized patient with acute dyspnea. We hypothesized that the addition of small‐group sessions would improve intern knowledge about and confidence in managing acute dyspnea above that gained from a combination of informal education and formal but lecture‐based education.

METHODS

Thirty‐eight internal medicine residents in their first year of postgraduate training (interns) at the University of Michigan were approached to participate in the study. Twenty‐six interns signed informed consent forms and were randomized using a random number generator to receive either the standard education (the control group) or the standard education plus the educational intervention (the intervention group). The standard education was informal teaching by senior medical residents on the wards and a 1‐hour lecture on Approach to the Patient with Acute Dyspnea, taught by an attending physician from the Department of Pulmonary and Critical Care Medicine. The educational intervention included the standard education as well as 2 small‐group, case‐based interactive sessions on acute dyspnea management. Both sessions were developed and taught by the first author (T.M.R.), a third‐year resident in internal medicine. A senior resident taught the sessions to try to make the information more relevant and practical and to make asking questions less intimidating. The first session, which lasted 50 minutes, discussed cases of bronchospasm, pulmonary edema, and pulmonary embolism as causes of acute dyspnea. It addressed several concepts: knowing when and how quickly to evaluate a dyspneic patient, formulating a differential diagnosis, appropriately evaluating acute dyspnea, providing empiric therapy, and recognizing indications for intubation. The second small‐group session occurred approximately 1 month after the first session and lasted 30 minutes. In this session key concepts learned during the first session were reviewed, and a case of ventricular tachycardia presenting as acute dyspnea was discussed. In an effort to increase attendance, free food and drink were provided at each session, and participants were sent reminders via e‐mail and the paging system prior to each session.

All study participants completed pre‐ and postintervention surveys that assessed their knowledge of acute dyspnea management and their confidence in managing patients with this condition. The pretests were conducted just before the first small‐group session was held. The post‐tests were conducted 4 months later. Knowledge was assessed by the score on the 45‐point test, which contained both open‐ and closed‐ended questions derived from 10 case‐based items. The number of points that a question was worth varied depending on how many elements made up a correct answer. For example, one question asked, What tests (if any) do you plan to order immediately after you examine the patient? As 3 tests should have been obtained (EKG, CXR, and ABG), this item had a maximum score of 3 points. Confidence was assessed by averaging 17 items scored on a 5‐point Likert scale (from strongly agree to strongly disagree). The items measured the physician's confidence in managing various aspects of the dyspneic patient (eg, confidence in knowing when to intubate a patient, when to obtain an ABG/CXR/EKG, and when to transfer a patient to the ICU). Data were analyzed using repeated‐measures analysis of variance. Primary analysis was based on the intention‐to‐treat principle, with alpha set to .05 (2‐sided). A secondary, per‐protocol analysis was also performed. In this analysis, study participants who attended both small‐group sessions (ie, completed the entire intervention) were compared with the control group. The protocol was approved by the institutional review board at the University of Michigan Health System.

RESULTS

All participants completed the study. Overall, only 3 of the 26 interns attended the lecture on Approach to the Patient with Acute Dyspnea. Fourteen of the 16 interns assigned to the intervention group attended 1 of the 2 small‐group sessions (11 attended the first session, and 10 attended the second session). Seven interns attended both sessions. The study period was 4 months. Both the intervention and control groups reported managing a similar number of patients with acute dyspnea, both prior to the study (mean of 5.9 in the intervention group and 7.4 in the control group, P = .51) and at the end of study (mean 10.6 in the intervention group and 10.2 in the control group, P = .91). There was no significant difference in the total number of completed inpatient months (mean of 4.9 in the intervention group and 4.7 in the control group, P =. 32) or in the number of inpatient months completed prior to the start of the study (mean of 2 in the intervention group and 2.4 in the control group, P = .15).

Confidence

Subjects in both the intervention and control groups showed increased confidence over time. The mean score of the intervention group increased from 3.77 to 4.57 (a 21.2% increase) and that of the control group increased from 3.74 to 4.28 (a 14.4% increase). Although the trend over time was highly significant for both groups (P < .001), the effect of the intervention was not significant (P = .19). However, the power to detect a difference between the groups was low (0.25). In the per‐protocol analysis, there was no significant difference between the groups (P = .26; see Fig. 1).

Figure 1
Change in confidence pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

Knowledge

In the primary analysis, results for knowledge were similar to those obtained for the confidence outcome. In the intervention group, the mean score increased from 35.6 to 38.3 (a 7.6% increase); in the control group, the mean increased from 36.2 to 38.2 (a 5.5% increase). Scores ranged from 31 to 42. Again, the trend for both groups was significant (P < .01), but the effect of the intervention was not significant (P = .65). The power to detect a difference between groups was again low (0.07). In the per‐protocol analysis a trend toward significance was seen, with mean scores increasing from 34.6 to 40.0, a 15.6% increase (P = .067; see Fig. 2).

Figure 2
Change in knowledge pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

DISCUSSION

Our randomized controlled trial found that intern confidence and knowledge about acute dyspnea management both increased significantly over time; however, no significant differences between the intervention and control groups were observed. The complete intervention was not administered to the vast majority of those in the intervention group, however, likely skewing results toward the null. As suggested by the per‐protocol analysis, there was a trend toward a significant increase in the knowledge of the interns who had received the entire intervention. This is similar to results found in a randomized study by Schroy et al., which demonstrated a significant increase in resident knowledge of colorectal cancer screening after an educational intervention that used an interactive, case‐based seminar.13

Our study had several strengths. First, we employed the most robust design to detect efficacy, a randomized controlled study design. Second, we had complete follow‐up because all participants finished the study. Finally, our intervention is easily reproducible.

Our findings should also be considered within the context of several limitations. Despite the use of a random number generator, the control and intervention groups were unequal in number, which may have affected the results, particularly with such a small sample size.

Second, the intervention did not occur until 3 months after the start of each participant's internship. The intention was to implement the intervention at the start of internship, but institutional review board approval did not occur for an additional 3 months. This late timing might have been unfortunate because interns may already have had an established management plan for acute dyspnea, making their behavior more difficult to alter, even with additional education.

Third, because we were unaware of available test instruments to assess resident knowledge of acute dyspnea in the hospitalized patient, we needed to create our own. Unfortunately, the instrument yielded only a small variance in test scores, which may have made it difficult to detect an effect on scores if present.

Fourth, attendance at each session was suboptimal, and thus the complete intervention was not administered to the vast majority of those in the intervention group. Because the first small‐group session was the main teaching session, interns who only attended the second session were exposed to just one case discussion and only a review, rather than a full formal discussion, of the material presented during the first session. Therefore, it is not known if the intervention really had no effect or if no differences were detected simply because the complete intervention was not received. The trend toward significance observed in the per‐protocol analysis suggests that compliance with the intervention may be the key to improving knowledge.

Given the small differences observed in this study, future interventions ideally should use a more sensitive testing instrument, a larger sample, and a more powerful intervention that occurs early in training. Future efforts should also be designed to improve attendance at educational interventions. In the setting of reduced resident work hours and increased demands on resident time, this will prove to be a true challenge for all educators and residency programs.

Cross‐cover is defined as an on‐call physician managing acute problems such as chest pain, dyspnea, and hypoxemia for patients primarily cared for by another physician. Cross‐cover problems are commonly encountered with hospitalized patients, and inappropriate evaluation and management can result in misdiagnosis. Residents in many internal medicine residency programs receive only informal instruction about how to manage cross‐cover problems, usually from senior medical residents. Unfortunately, instruction is often provided while a patient is experiencing a problem, a frequent occurrence in the chaotic circumstances of a stressful learning environment. Furthermore, the knowledge base, experience, and teaching skills of senior residents vary substantially, and typically senior residents receive no formal instruction to guide them in how or what to teach more junior residents. If formal instruction is provided to residents, it is typically through often poorly attended didactic lectures that have been shown to be an ineffective forum for acquiring skills or changing physician behavior.15

Although previous studies did find that educational interventions can improve confidence and increase knowledge about various aspects of residency training, many of these studies were not randomized,68 or they involved complex interventions requiring a significant amount of resident and teaching staff time.911 The few randomized studies that used simple educational interventions focused on outpatient education, but most of a resident's time is spent in an inpatient setting.1213

Therefore, we designed a simple, randomized educational intervention consisting of 2 formal small‐group, case‐based discussion sessions addressing 1 cross‐cover situation: a hospitalized patient with acute dyspnea. We hypothesized that the addition of small‐group sessions would improve intern knowledge about and confidence in managing acute dyspnea above that gained from a combination of informal education and formal but lecture‐based education.

METHODS

Thirty‐eight internal medicine residents in their first year of postgraduate training (interns) at the University of Michigan were approached to participate in the study. Twenty‐six interns signed informed consent forms and were randomized using a random number generator to receive either the standard education (the control group) or the standard education plus the educational intervention (the intervention group). The standard education was informal teaching by senior medical residents on the wards and a 1‐hour lecture on Approach to the Patient with Acute Dyspnea, taught by an attending physician from the Department of Pulmonary and Critical Care Medicine. The educational intervention included the standard education as well as 2 small‐group, case‐based interactive sessions on acute dyspnea management. Both sessions were developed and taught by the first author (T.M.R.), a third‐year resident in internal medicine. A senior resident taught the sessions to try to make the information more relevant and practical and to make asking questions less intimidating. The first session, which lasted 50 minutes, discussed cases of bronchospasm, pulmonary edema, and pulmonary embolism as causes of acute dyspnea. It addressed several concepts: knowing when and how quickly to evaluate a dyspneic patient, formulating a differential diagnosis, appropriately evaluating acute dyspnea, providing empiric therapy, and recognizing indications for intubation. The second small‐group session occurred approximately 1 month after the first session and lasted 30 minutes. In this session key concepts learned during the first session were reviewed, and a case of ventricular tachycardia presenting as acute dyspnea was discussed. In an effort to increase attendance, free food and drink were provided at each session, and participants were sent reminders via e‐mail and the paging system prior to each session.

All study participants completed pre‐ and postintervention surveys that assessed their knowledge of acute dyspnea management and their confidence in managing patients with this condition. The pretests were conducted just before the first small‐group session was held. The post‐tests were conducted 4 months later. Knowledge was assessed by the score on the 45‐point test, which contained both open‐ and closed‐ended questions derived from 10 case‐based items. The number of points that a question was worth varied depending on how many elements made up a correct answer. For example, one question asked, What tests (if any) do you plan to order immediately after you examine the patient? As 3 tests should have been obtained (EKG, CXR, and ABG), this item had a maximum score of 3 points. Confidence was assessed by averaging 17 items scored on a 5‐point Likert scale (from strongly agree to strongly disagree). The items measured the physician's confidence in managing various aspects of the dyspneic patient (eg, confidence in knowing when to intubate a patient, when to obtain an ABG/CXR/EKG, and when to transfer a patient to the ICU). Data were analyzed using repeated‐measures analysis of variance. Primary analysis was based on the intention‐to‐treat principle, with alpha set to .05 (2‐sided). A secondary, per‐protocol analysis was also performed. In this analysis, study participants who attended both small‐group sessions (ie, completed the entire intervention) were compared with the control group. The protocol was approved by the institutional review board at the University of Michigan Health System.

RESULTS

All participants completed the study. Overall, only 3 of the 26 interns attended the lecture on Approach to the Patient with Acute Dyspnea. Fourteen of the 16 interns assigned to the intervention group attended 1 of the 2 small‐group sessions (11 attended the first session, and 10 attended the second session). Seven interns attended both sessions. The study period was 4 months. Both the intervention and control groups reported managing a similar number of patients with acute dyspnea, both prior to the study (mean of 5.9 in the intervention group and 7.4 in the control group, P = .51) and at the end of study (mean 10.6 in the intervention group and 10.2 in the control group, P = .91). There was no significant difference in the total number of completed inpatient months (mean of 4.9 in the intervention group and 4.7 in the control group, P =. 32) or in the number of inpatient months completed prior to the start of the study (mean of 2 in the intervention group and 2.4 in the control group, P = .15).

Confidence

Subjects in both the intervention and control groups showed increased confidence over time. The mean score of the intervention group increased from 3.77 to 4.57 (a 21.2% increase) and that of the control group increased from 3.74 to 4.28 (a 14.4% increase). Although the trend over time was highly significant for both groups (P < .001), the effect of the intervention was not significant (P = .19). However, the power to detect a difference between the groups was low (0.25). In the per‐protocol analysis, there was no significant difference between the groups (P = .26; see Fig. 1).

Figure 1
Change in confidence pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

Knowledge

In the primary analysis, results for knowledge were similar to those obtained for the confidence outcome. In the intervention group, the mean score increased from 35.6 to 38.3 (a 7.6% increase); in the control group, the mean increased from 36.2 to 38.2 (a 5.5% increase). Scores ranged from 31 to 42. Again, the trend for both groups was significant (P < .01), but the effect of the intervention was not significant (P = .65). The power to detect a difference between groups was again low (0.07). In the per‐protocol analysis a trend toward significance was seen, with mean scores increasing from 34.6 to 40.0, a 15.6% increase (P = .067; see Fig. 2).

Figure 2
Change in knowledge pre‐ and postintervention. Number of participating interns in each group: control, 10; intervention, 16; per‐protocol, 7.

DISCUSSION

Our randomized controlled trial found that intern confidence and knowledge about acute dyspnea management both increased significantly over time; however, no significant differences between the intervention and control groups were observed. The complete intervention was not administered to the vast majority of those in the intervention group, however, likely skewing results toward the null. As suggested by the per‐protocol analysis, there was a trend toward a significant increase in the knowledge of the interns who had received the entire intervention. This is similar to results found in a randomized study by Schroy et al., which demonstrated a significant increase in resident knowledge of colorectal cancer screening after an educational intervention that used an interactive, case‐based seminar.13

Our study had several strengths. First, we employed the most robust design to detect efficacy, a randomized controlled study design. Second, we had complete follow‐up because all participants finished the study. Finally, our intervention is easily reproducible.

Our findings should also be considered within the context of several limitations. Despite the use of a random number generator, the control and intervention groups were unequal in number, which may have affected the results, particularly with such a small sample size.

Second, the intervention did not occur until 3 months after the start of each participant's internship. The intention was to implement the intervention at the start of internship, but institutional review board approval did not occur for an additional 3 months. This late timing might have been unfortunate because interns may already have had an established management plan for acute dyspnea, making their behavior more difficult to alter, even with additional education.

Third, because we were unaware of available test instruments to assess resident knowledge of acute dyspnea in the hospitalized patient, we needed to create our own. Unfortunately, the instrument yielded only a small variance in test scores, which may have made it difficult to detect an effect on scores if present.

Fourth, attendance at each session was suboptimal, and thus the complete intervention was not administered to the vast majority of those in the intervention group. Because the first small‐group session was the main teaching session, interns who only attended the second session were exposed to just one case discussion and only a review, rather than a full formal discussion, of the material presented during the first session. Therefore, it is not known if the intervention really had no effect or if no differences were detected simply because the complete intervention was not received. The trend toward significance observed in the per‐protocol analysis suggests that compliance with the intervention may be the key to improving knowledge.

Given the small differences observed in this study, future interventions ideally should use a more sensitive testing instrument, a larger sample, and a more powerful intervention that occurs early in training. Future efforts should also be designed to improve attendance at educational interventions. In the setting of reduced resident work hours and increased demands on resident time, this will prove to be a true challenge for all educators and residency programs.

References
  1. Carney PA,Dietrich AJ,Freeman DH,Mott LA.A standardized‐patient assessment of a continuing medical education program to improve physicians' cancer‐control clinical skills.Acad Med.1995;70(1):5258.
  2. Roche AM,Eccleston P,Sanson‐Fisher R.Teaching smoking cessation skills to senior medical students: a block‐randomized controlled trial of four different approaches.Prev Med.1996;25:251258.
  3. Davis D,O'Brien MA,Freemantle N,Wolf FM,Mazmanian P,Taylor‐Vaisey A.Impact of formal continuing medical education: Do conferences, workshops, rounds, and other traditional continuing education activities change physician behavior or health care outcomes?JAMA.1999;282:867874.
  4. Smits PB,de Buisonje CD,Verbeek JH,van Dijk FJ,Metz JC,ten Cate OJ.Problem‐based learning versus lecture‐based learning in postgraduate medical education.Scand J Work Environ Health.2003;29:280287.
  5. Herbert CP,Wright JM,Maclure M,Wakefield J,Dormuth C,Brett‐MacLean P,Legare J,Premi J.Better Prescribing Project: A randomized controlled trial of the impact of case‐based educational modules and personal prescribing feedback on prescribing for hypertension in primary care.Family Pract.2004;21:575581.
  6. Hillenbrand KM,Larsen PG.Effect of an educational intervention about breastfeeding on the knowledge, confidence, and behaviors of pediatric resident physicians.Pediatrics.2002;110(5):e59.
  7. Learman LA,Gerrity MS,Field DR,van Blaricom A,Romm J,Choe J.Effects of a depression education program on residents' knowledge, attitudes, and clinical skills.Obstet Gynecol.2003;101(1):167174.
  8. Meier AH,Henry J,Marine R,Murray WB.Implementation of a web‐ and simulation‐based curriculum to ease the transition from medical school to surgical internship.Am J Surg.2005;190(1):137140.
  9. Smith RC,Lyles JS,Mettler J, et al.The effectiveness of intensive training for residents in interviewing.Ann Intern Med.1998;128(2):118126.
  10. Murdoch Eaton D,Cottrell D.Structured teaching methods enhance skill acquisition but not problem‐solving abilities: an evaluation of the “silent run through.”Med Educ.1999;33:019023.
  11. Abraham A,Cheng T,Wright J,Addlestone I,Huang Z,Greenberg L.An educational intervention to improve physician violence screening skills.Pediatrics.2001;107(5):e68.
  12. D'Onofrio G,Nadel ES,Degutis LC,Sullivan LM,Casper K,Bernstein E,Samet JH.Improving emergency medicine residents' approach to patients with alcohol problems: a controlled educational trial.Ann Emerg Med.2002;40(1):5062.
  13. Schroy PC,Glick JT,Geller AC,Jackson A,Heeren T,Prout M.A novel educational strategy to enhance internal medicine residents' familial colorectal cancer knowledge and risk assessment skills.Am J Gastroenterol.2005;100:677684.
References
  1. Carney PA,Dietrich AJ,Freeman DH,Mott LA.A standardized‐patient assessment of a continuing medical education program to improve physicians' cancer‐control clinical skills.Acad Med.1995;70(1):5258.
  2. Roche AM,Eccleston P,Sanson‐Fisher R.Teaching smoking cessation skills to senior medical students: a block‐randomized controlled trial of four different approaches.Prev Med.1996;25:251258.
  3. Davis D,O'Brien MA,Freemantle N,Wolf FM,Mazmanian P,Taylor‐Vaisey A.Impact of formal continuing medical education: Do conferences, workshops, rounds, and other traditional continuing education activities change physician behavior or health care outcomes?JAMA.1999;282:867874.
  4. Smits PB,de Buisonje CD,Verbeek JH,van Dijk FJ,Metz JC,ten Cate OJ.Problem‐based learning versus lecture‐based learning in postgraduate medical education.Scand J Work Environ Health.2003;29:280287.
  5. Herbert CP,Wright JM,Maclure M,Wakefield J,Dormuth C,Brett‐MacLean P,Legare J,Premi J.Better Prescribing Project: A randomized controlled trial of the impact of case‐based educational modules and personal prescribing feedback on prescribing for hypertension in primary care.Family Pract.2004;21:575581.
  6. Hillenbrand KM,Larsen PG.Effect of an educational intervention about breastfeeding on the knowledge, confidence, and behaviors of pediatric resident physicians.Pediatrics.2002;110(5):e59.
  7. Learman LA,Gerrity MS,Field DR,van Blaricom A,Romm J,Choe J.Effects of a depression education program on residents' knowledge, attitudes, and clinical skills.Obstet Gynecol.2003;101(1):167174.
  8. Meier AH,Henry J,Marine R,Murray WB.Implementation of a web‐ and simulation‐based curriculum to ease the transition from medical school to surgical internship.Am J Surg.2005;190(1):137140.
  9. Smith RC,Lyles JS,Mettler J, et al.The effectiveness of intensive training for residents in interviewing.Ann Intern Med.1998;128(2):118126.
  10. Murdoch Eaton D,Cottrell D.Structured teaching methods enhance skill acquisition but not problem‐solving abilities: an evaluation of the “silent run through.”Med Educ.1999;33:019023.
  11. Abraham A,Cheng T,Wright J,Addlestone I,Huang Z,Greenberg L.An educational intervention to improve physician violence screening skills.Pediatrics.2001;107(5):e68.
  12. D'Onofrio G,Nadel ES,Degutis LC,Sullivan LM,Casper K,Bernstein E,Samet JH.Improving emergency medicine residents' approach to patients with alcohol problems: a controlled educational trial.Ann Emerg Med.2002;40(1):5062.
  13. Schroy PC,Glick JT,Geller AC,Jackson A,Heeren T,Prout M.A novel educational strategy to enhance internal medicine residents' familial colorectal cancer knowledge and risk assessment skills.Am J Gastroenterol.2005;100:677684.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
339-343
Page Number
339-343
Article Type
Display Headline
What effect does an educational intervention have on interns' confidence and knowledge regarding acute dyspnea management?. A randomized controlled trial
Display Headline
What effect does an educational intervention have on interns' confidence and knowledge regarding acute dyspnea management?. A randomized controlled trial
Legacy Keywords
medical education, dyspnea, diagnostic error, respiratory tract diseases
Legacy Keywords
medical education, dyspnea, diagnostic error, respiratory tract diseases
Sections
Article Source

Copyright © 2006 Society of Hospital Medicine

Disallow All Ads
Correspondence Location
Cogent Healthcare of Iowa, St. Luke's Hospital, 1026 A Avenue NE, Cedar Rapids, IA 52406‐3026; Fax: (319) 368‐5973
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Article PDF Media

Transition of Care for Hospitalized Elderly

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
Transition of care for hospitalized elderly patients—Development of a discharge checklist for hospitalists

Hospital discharge is a critical transition point for many inpatients. Patient recovery from diseases requiring hospitalization is frequently incomplete and requires ongoing management and evaluation after discharge. For hospitalists who focus their practice primarily on inpatient care, the handoff to the outpatient setting frequently involves a change in health care provider and care team. Changes in care environment and care goals can lead to adverse patient‐ and system‐level events.1 High‐risk patients with multiple medical issues and elderly patients are especially vulnerable to the consequences of ineffective discharge handoffs.2, 3

Several studies have identified the errors that commonly occur around the time of hospital discharge. Forster et al.4 found that 1 in 5 patients experiences an adverse event (defined as an injury resulting from medical management rather than from the underlying disease) in the transition from hospital to home. They also found that approximately 62% of adverse events could be either prevented or ameliorated.4 Roy et al. examined test results pending at the time of discharge and determined that posthospital providers were frequently unaware of pending test results, with a potentially serious clinical impact.5 In an analysis of adverse events at 2 large hospitals in the United Kingdom, Neale et al. found that almost 11% of those hospitalized had an adverse event, 18% of which were attributable to the discharge process.6

Communication of important transitional care issues to the posthospital care team and to the patient is essential to a safe transition. Studies by van Walraven et al. found that patient follow‐up with a physician who had access to the hospital discharge summary was associated with a decreased risk of rehospitalization.7 Patients not understanding discharge medications,8 dietary restrictions, or other lifestyle changes such as smoking cessation and exercise can lead to ineffective care transitions. Furthermore, the health system's barriers to effective patient self‐management may exacerbate the risk in the transition from the hospital setting.2, 913

In addition to the growing research literature that has identified gaps in the discharge process, the Joint Commission for the Accreditation of Healthcare Organizations (JCAHO) has included discharge instructions as a core performance measure in the care of heart failure patients. Hospital performance on this measure is reported publicly on the Centers for Medicare and Medicaid Services website (www.hospitalcompare.hhs.gov). Furthermore, the 2006 JCAHO patient safety goal of medication reconciliation recognizes the importance of preventing lapses in medication safety at points of care transition.14, 15 JCAHO now requires the development and implementation of processes to collect, review, reconcile, and document prescribed medications at all points of care transition, including hospital discharge.16

Older adults are considered more vulnerable to adverse events after discharge.8 They account for approximately 12% of the total U.S. population, but they make up 70% of hospitalized patients.17 With these factors in mind, the Society of Hospital Medicine (SHM) identified the elderly as a group especially vulnerable to the clinical care handoffs that occur in the hospital discharge process and therefore the patient population targeted in constructing the required elements of an ideal hospital discharge.

In addition to identifying a target patient population, inclusion of stakeholders primarily responsible for implementation is critical to developing a new process standard. In this instance, the hospitalist was identified as a critical architect of the development of the ideal discharge process, although clearly the hospitalist is just one of many people ultimately responsible for coordinating an effective hospital discharge. Finally, the organizations within which the elderly receive care and at which hospitalists practice are important partners in the implementation of systems of care that facilitate seamless care transitions.

In examining the myriad stakeholders involved in the discharge transitionthe patient, the hospitalist, other caregivers involved in hospital care, and the organizationSHM's Hospital Quality & Patient Safety (HQPS) Committee undertook an initiative to develop a practical list of important elements for hospitalists to include in the discharge of elderly inpatients, referred to in this article as the discharge checklist.

METHODS

In a process similar to that used by professional societies in the development of clinical guidelines, the SHM HQPS Committee used a combination of evidence‐based review and expert panels to develop a discharge checklist for elderly patients. Given that the focus of this project was a process improvement rather than a specific clinical condition, the SHM also believed it was critical to share the draft checklist with academic and community‐based practitioners knowledgeable in both the myriad logistical issues of and potential barriers to improving the discharge transition. The detailed process for checklist development is outlined below and summarized in Figure 1.

Figure 1
Process of development of the discharge checklist.

Literature Review

A Medline search was performed using the keywords patient discharge and either quality indicators, health care, or quality of health care. Articles included were those written in English and published between January 1975 and January 2005. We also reviewed the abstracts submitted to the SHM's 2003‐2005 annual and regional meetings in and reviewed those that included the designated keywords in their content focus. The number of articles selected was narrowed from 274 to 32 by including only studies of specific discharge elements, articles describing adverse events associated with but not including specific discharge elements, descriptions of tools to gather and report important data at the time of hospital discharge, or recommendations of experts or medical associations about methods of improving the discharge process.

DRAFT Checklist and Expert Review

Two members of the discharge checklist team (S.K. and D.M.) reviewed all 32 relevant reports and assembled a list of possible items for inclusion in an ideal hospital discharge. Inclusion of items was based on clinical relevance to elderly patients and impact on postdischarge care. This list initially contained 24 items in 3 domainsdischarge planning, medications, and the discharge summary document.

The list was sent to 3 experts, selected on the basis of their academic expertise in the fields of geriatrics and care transitions. Each independently reviewed the list, and then all 3 experts met several times by conference call. Items approved by at least 2 of the 3 experts were retained. The revised checklist transformed the 3 domains originally identified into 9 main elements, each with 2‐5 subelements.

Peer Review at SHM Annual Meeting

In a workshop at the 2005 SHM Annual Meeting, a facilitator presented the checklist and moderated a discussion among several experts from the task force and expert panel. The expert panel shared relevant background literature and key findings from their own research. Audience members included community and academic hospitalists, case managers, and pharmacists. Many attendees responded to the checklist and raised relevant issues. In all, 120 clinicians participated in this 90‐minute workshop.

After reviewing the checklist, workshop attendees gave both formal and informal input into the checklist content. Through group discussion and individual suggestions, items were added to the checklist. This process resulted in the addition of 1 main element and 3 subelements. At its completion, each workshop participant was allowed up to 3 votes for items that they believed should be removed from the modified checklist. The results were tallied, and the checklist was further reviewed and critiqued by the workshop faculty. Elements of the discharge checklist were designated as required for optimal handoffs if there was consensus among the committee members and workshop attendees. Elements that did not have unanimous support were discussed further and designated as optional. The final checklist was then developed with both required and optional elements and endorsed by the HQPS Committee and the SHM board.

RESULTS

The final discharge checklist is shown in Figure 2. It contains required and optional data elements and processes for 3 types of discharge documents: the discharge summary, patient instructions, and communication (by phone, e‐mail, or fax) on the day of discharge to the receiving provider. Other documents, such as transfer orders for a rehabilitation facility or nursing home, were considered outside the scope of this project.

Figure 2
Ideal discharge of the elderly patient: a hospitalist checklist. x = required element; o = optional element.

The literature review identified medications as a significant source of adverse events for patients upon hospital discharge.4, 8, 14, 1820 The expert panel and workshop participants all endorsed the need for additional detailed attention to reviewing and reconciling medications during the discharge process. The use of standardized tools was suggested by the group to improve the medication review process.21 The required elements include not only a list of discharge medications but also attention to high‐risk medications that require closer postdischarge follow‐up and monitoring (such as warfarin,22 diuretics, nephrotoxic medications, corticosteroids, hypoglycemic medications, and narcotic analgesics), reconciliation of the discharge medication regimen with preadmission medications and designation of medications as new, modified, or discontinued,23 and emphasis on assessing patient understanding of medication self‐management plans.24 Several published studies found that pharmacist oversight of discharge medications or postdischarge telephone calls improved patient outcomes.1820 However, not every health system has the resources and infrastructure necessary to implement these types of programs. Moreover, methods of implementation of each of these discharge elements were believed to be beyond the scope of this project, so pharmacist involvement was not specifically included in this checklist.

The expert panel and workshop participants found items related to cognition and functional status to be important for patients whose usual cognitive or functional status was changed or whose status at discharge was not within normal limits.25, 26 Clinicians seeing patients in follow‐up would then have an important reference point for evaluating progress and the need for additional home support or therapy. Patients with limited literacy or language barriers may need these issues assessed with the help of family members and/or translators to identify changes from their baseline level of functioning.

In addition, resuscitation status was viewed by the group as an important data element for some patients,27 particularly those who had been critically ill. Development of disease or population‐specific content, for example, for patients with heart failure or pneumonia, was also identified as critical to the safe discharge of elderly patient, with the understanding that there may be a need to modify and individualize the content for patients with complex conditions and multiple comorbidities.

The content of the hospital discharge summary deemphasized the need for a complete history of the present illness at the time of hospital admission or an exhaustive hospital course. Instead, it highlighted the need to identify a patient's condition at discharge, pending issues and interventions requiring ongoing and focused monitoring, contingency planning, and contact information of knowledgeable providers in case questions arise after discharge.2830

Postdischarge care was emphasized with the need for a follow‐up appointment within at most 2 weeks of discharge or sooner for patients with fragile clinical conditions.31 Although this was not recommended because of a published study, it was the consensus of the expert panel and peer review process that close follow‐up after hospital discharge was critical in ensuring medication safety. Transportation limitations and other logistical problems with access to a follow‐up clinician were identified as important issues to be resolved in the discharge planning process in order for timely follow‐up to occur. In addition, it was deemed critical that the follow‐up provider receive the key information about the hospitalization with any necessary follow‐up instructions as soon after discharge as possible13 and certainly before the first postdischarge visit. Instructions to patients about medication schedules and follow‐up care need to be in writing at a 6th‐grade reading level; furthermore, processes to identify a patient's level of understanding of the follow‐up plan and areas for targeted education need to be established.24

DISCUSSION

We believe the development of a checklist of required elements to be communicated at discharge is a key step toward standardizing the hospital discharge process. The checklist highlights what is believed to be the key information about the transition of care and its process. The checklist is intended to standardize what is required for a successful hospital discharge. However, each institution will need to further refine this list according to local factors such as patient population, resources, and culture and to determine how best to implement the necessary changes to their current discharge process. Local modification of the checklist also allows for the addition of other elements that are patient‐ or population specific. Elderly patients discharged home from the hospital are the primary patient population targeted by this checklist ; there may be unique and additional elements necessary for an ideal discharge for a patient who is discharged to a subacute or acute rehabilitation facility. These elements are not described in this checklist but will be the focus of future work.

Establishing the critical elements of a hospital discharge transition sets the stage for improving patient outcomes in the immediate postdischarge period. Most important, the checklist conveys the message that the discharge process requires critical thinking, collaboration, and goal setting and that this coordination of care takes time. However, the discharge checklist must reside within a hospital culture that in general does not value the discharge process in the same way it values the admission process. The latter is more standardized and incorporates expectations about content and communication. In the same way, the current discharge is an admission to the next health care setting and deserves at least as much time and effort as a hospital admission. Furthermore, if institutions examine their current discharge processes, they may find that the time necessary to complete the discharge may be similar to the time necessary to admit a patient to the hospital. Finally, organizations need to develop internal policies and procedures that monitor and provide feedback about important dimensions of the discharge process, including content, patient understanding, information transfer, and clinical and service outcomes including satisfaction of the patient and the postdischarge provider. Hospital discharge is truly a team process involving nurses, pharmacists, case managers, and other hospital personnel, so performance measurement should be at the team or unit level, unlike other areas for which individual physicians may receive feedback on performance.

The limitations of the checklist development process include the paucity of randomized, controlled trials focused on the study of health care delivery processes and the lack of an industry gold standard. Furthermore, the heterogeneity of health care delivery systems makes it difficult to recommend specific interventions without understanding the myriad local issues. Those who provided input into this checklist included members of the inpatient team, a scope that can be broadened in the future to include outpatient physicians, patients, and caregivers in the home and long‐term care environments. However, the elements defined through the checklist serve as a starting point for developing discharge transition standards for older adults.

As leaders in hospital care, hospitalists are positioned to raise awareness of the importance of hospital discharge and to lead multidisciplinary efforts to improve the discharge process within their organizations. The first step in that process should be understanding the required elements and local facilitating factors and barriers in achieving a predictable, seamless transition of care for hospitalized patients.

References
  1. Cook RI,Render M,Woods DD.Gaps in the continuity of care and progress on patient safety.BMJ.2000;320:791794.
  2. Bull MJ,Hansen HE,Gross CR.Predictors of elder and family caregiver satisfaction with discharge planning.J Cardiovasc Nurs.2000;14:7687.
  3. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders: a randomized clinical trial.JAMA.1999;281:613620.
  4. Forster AJ,Murff HJ,Peterson JF, et al.The incidence and severity of adverse events affecting patients after discharge from the hospital.Ann Intern Med.2003;138:161167.
  5. Roy C,Poon EG,Karson AS, et al.Patient safety concerns arising from test results that return after hospital discharge.Ann Intern Med.2005;143:121128.
  6. Neale G,Woloshynowych M,Vincent C.Exploring the causes of adverse events in NHS hospital practice.J. R. Soc Med.2001;94:553.
  7. van Walraven C,Seth R,Austin PC,Laupacis A.Effect of discharge summary availability during the post‐discharge visits on hospital readmission.J Gen Intern Med.2002;17:186192.
  8. Martens KH.An ethnographic study of the process of medication discharge education (MDE).J Adv Nurs.1998;27:341348.
  9. Cleary PD.A hospitalization from hell: a patient's perspective on quality.Ann Intern Med.2003;138:3339.
  10. Demlo LK,Campbell PM.Improving discharge data: lessons from the National Hospital Discharge Survey.Med Care1981;19:10301040.
  11. Felden JM,Scott S,Horne JG.An investigation of patient satisfaction following discharge after total hip replacement surgery.Orthop Nurs.2003;22:429436.
  12. Hickey ML,Kleefield SF,Pearson SD, et al.Payer‐hospital collaboration to improve patient satisfaction with hospital discharge.Jt Comm J QuaI Improv.1996;22:336344.
  13. van Walraven C,Mamdani M,Fang J,Austin PC.Continuity of care and patient outcomes after hospital discharge.J Gen Intern Med.2004;19:624631.
  14. Resar R.Will, ideas, and execution: their role in reducing adverse medication events.J Pediatr.2005;147:727728.
  15. Resar R.Why we need to learn standardisation.Aust Fam Physician.2005;34(1‐2):6768.
  16. Joint Commission on Accreditation of Healthcare Organizations.2006 Critical Access Hospital and Hospital National Patient Safety Goals. Available at: http://www.jcaho.org/accredited+organizations/patient+safety/06_npsg/06_npsg_cah_hap.htm.
  17. Census Bureau of Statistics,2000.
  18. Kucukarslan S,Peters M,Mlynarek , et al.Pharmacists on rounding teams reduce preventable adverse events in hospital general medicine units.Arch Intern Med.2003;163:20142018.
  19. Dudas V,Bookwalter T,Kerr K, et al.The impact of follow‐up telephone calls to patients after hospitalization.Ann Intern Med.2001;111(9B):26S30S.
  20. Schnipper JL,Kirwin JL,Cotugno MC, et al.Role of pharmacist counseling in preventing adverse drug events after hospitalization.Arch Intern Med.2006;166:565571.
  21. Lewis T.Using the NO TEARS tool for medication review.BMJ.2004;329:434.
  22. Manning DM.Toward safer warfarin therapy: does precise daily dosing improve INR control?Mayo Clinic Proc.2002;77:873875.
  23. Resar R.Institute for Healthcare Improvement, personal communication.
  24. Institute of Medicine.Kindig DA, editor.Health Literacy: A Prescription to End Confusion.Washington, DC:National Academies Press,2004.
  25. Manning DM,Keller AS,Frank DL.Independent Mobility Validation Exam (I‐MOVE): a tool for periodic reassessment of fall‐risk and discharge planning. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
  26. Mathias S,Nayak US,Isaacs B.Balance in elderly patients: the “get‐up‐and‐go” test.Arch Phys Med Rehabil.1986;67:387389.
  27. AMA, Council on Ethical and Judicial Affairs.Guidelines for appropriate use of “do‐not‐resuscitate” orders.JAMA.1991;265:18681871.
  28. van Walraven C,Weinberg AL.Quality assessment of a discharge summary system.CMAJ.1995;152:14371442.
  29. van Walraven C,Rokosh E.What is necessary for high‐quality discharge summaries?Am J Med Qual.1999.14:160169.
  30. JCAHO Manual: Information Management (IM) 6.10 and Patient Care (PC) 15.30
  31. Whitford K,Huddleston JM.Specific appointments after pneumonia hospitalization reduce readmissions. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
354-360
Legacy Keywords
care standardization, continuity of care transition and discharge planning, multidisciplinary care
Sections
Article PDF
Article PDF

Hospital discharge is a critical transition point for many inpatients. Patient recovery from diseases requiring hospitalization is frequently incomplete and requires ongoing management and evaluation after discharge. For hospitalists who focus their practice primarily on inpatient care, the handoff to the outpatient setting frequently involves a change in health care provider and care team. Changes in care environment and care goals can lead to adverse patient‐ and system‐level events.1 High‐risk patients with multiple medical issues and elderly patients are especially vulnerable to the consequences of ineffective discharge handoffs.2, 3

Several studies have identified the errors that commonly occur around the time of hospital discharge. Forster et al.4 found that 1 in 5 patients experiences an adverse event (defined as an injury resulting from medical management rather than from the underlying disease) in the transition from hospital to home. They also found that approximately 62% of adverse events could be either prevented or ameliorated.4 Roy et al. examined test results pending at the time of discharge and determined that posthospital providers were frequently unaware of pending test results, with a potentially serious clinical impact.5 In an analysis of adverse events at 2 large hospitals in the United Kingdom, Neale et al. found that almost 11% of those hospitalized had an adverse event, 18% of which were attributable to the discharge process.6

Communication of important transitional care issues to the posthospital care team and to the patient is essential to a safe transition. Studies by van Walraven et al. found that patient follow‐up with a physician who had access to the hospital discharge summary was associated with a decreased risk of rehospitalization.7 Patients not understanding discharge medications,8 dietary restrictions, or other lifestyle changes such as smoking cessation and exercise can lead to ineffective care transitions. Furthermore, the health system's barriers to effective patient self‐management may exacerbate the risk in the transition from the hospital setting.2, 913

In addition to the growing research literature that has identified gaps in the discharge process, the Joint Commission for the Accreditation of Healthcare Organizations (JCAHO) has included discharge instructions as a core performance measure in the care of heart failure patients. Hospital performance on this measure is reported publicly on the Centers for Medicare and Medicaid Services website (www.hospitalcompare.hhs.gov). Furthermore, the 2006 JCAHO patient safety goal of medication reconciliation recognizes the importance of preventing lapses in medication safety at points of care transition.14, 15 JCAHO now requires the development and implementation of processes to collect, review, reconcile, and document prescribed medications at all points of care transition, including hospital discharge.16

Older adults are considered more vulnerable to adverse events after discharge.8 They account for approximately 12% of the total U.S. population, but they make up 70% of hospitalized patients.17 With these factors in mind, the Society of Hospital Medicine (SHM) identified the elderly as a group especially vulnerable to the clinical care handoffs that occur in the hospital discharge process and therefore the patient population targeted in constructing the required elements of an ideal hospital discharge.

In addition to identifying a target patient population, inclusion of stakeholders primarily responsible for implementation is critical to developing a new process standard. In this instance, the hospitalist was identified as a critical architect of the development of the ideal discharge process, although clearly the hospitalist is just one of many people ultimately responsible for coordinating an effective hospital discharge. Finally, the organizations within which the elderly receive care and at which hospitalists practice are important partners in the implementation of systems of care that facilitate seamless care transitions.

In examining the myriad stakeholders involved in the discharge transitionthe patient, the hospitalist, other caregivers involved in hospital care, and the organizationSHM's Hospital Quality & Patient Safety (HQPS) Committee undertook an initiative to develop a practical list of important elements for hospitalists to include in the discharge of elderly inpatients, referred to in this article as the discharge checklist.

METHODS

In a process similar to that used by professional societies in the development of clinical guidelines, the SHM HQPS Committee used a combination of evidence‐based review and expert panels to develop a discharge checklist for elderly patients. Given that the focus of this project was a process improvement rather than a specific clinical condition, the SHM also believed it was critical to share the draft checklist with academic and community‐based practitioners knowledgeable in both the myriad logistical issues of and potential barriers to improving the discharge transition. The detailed process for checklist development is outlined below and summarized in Figure 1.

Figure 1
Process of development of the discharge checklist.

Literature Review

A Medline search was performed using the keywords patient discharge and either quality indicators, health care, or quality of health care. Articles included were those written in English and published between January 1975 and January 2005. We also reviewed the abstracts submitted to the SHM's 2003‐2005 annual and regional meetings in and reviewed those that included the designated keywords in their content focus. The number of articles selected was narrowed from 274 to 32 by including only studies of specific discharge elements, articles describing adverse events associated with but not including specific discharge elements, descriptions of tools to gather and report important data at the time of hospital discharge, or recommendations of experts or medical associations about methods of improving the discharge process.

DRAFT Checklist and Expert Review

Two members of the discharge checklist team (S.K. and D.M.) reviewed all 32 relevant reports and assembled a list of possible items for inclusion in an ideal hospital discharge. Inclusion of items was based on clinical relevance to elderly patients and impact on postdischarge care. This list initially contained 24 items in 3 domainsdischarge planning, medications, and the discharge summary document.

The list was sent to 3 experts, selected on the basis of their academic expertise in the fields of geriatrics and care transitions. Each independently reviewed the list, and then all 3 experts met several times by conference call. Items approved by at least 2 of the 3 experts were retained. The revised checklist transformed the 3 domains originally identified into 9 main elements, each with 2‐5 subelements.

Peer Review at SHM Annual Meeting

In a workshop at the 2005 SHM Annual Meeting, a facilitator presented the checklist and moderated a discussion among several experts from the task force and expert panel. The expert panel shared relevant background literature and key findings from their own research. Audience members included community and academic hospitalists, case managers, and pharmacists. Many attendees responded to the checklist and raised relevant issues. In all, 120 clinicians participated in this 90‐minute workshop.

After reviewing the checklist, workshop attendees gave both formal and informal input into the checklist content. Through group discussion and individual suggestions, items were added to the checklist. This process resulted in the addition of 1 main element and 3 subelements. At its completion, each workshop participant was allowed up to 3 votes for items that they believed should be removed from the modified checklist. The results were tallied, and the checklist was further reviewed and critiqued by the workshop faculty. Elements of the discharge checklist were designated as required for optimal handoffs if there was consensus among the committee members and workshop attendees. Elements that did not have unanimous support were discussed further and designated as optional. The final checklist was then developed with both required and optional elements and endorsed by the HQPS Committee and the SHM board.

RESULTS

The final discharge checklist is shown in Figure 2. It contains required and optional data elements and processes for 3 types of discharge documents: the discharge summary, patient instructions, and communication (by phone, e‐mail, or fax) on the day of discharge to the receiving provider. Other documents, such as transfer orders for a rehabilitation facility or nursing home, were considered outside the scope of this project.

Figure 2
Ideal discharge of the elderly patient: a hospitalist checklist. x = required element; o = optional element.

The literature review identified medications as a significant source of adverse events for patients upon hospital discharge.4, 8, 14, 1820 The expert panel and workshop participants all endorsed the need for additional detailed attention to reviewing and reconciling medications during the discharge process. The use of standardized tools was suggested by the group to improve the medication review process.21 The required elements include not only a list of discharge medications but also attention to high‐risk medications that require closer postdischarge follow‐up and monitoring (such as warfarin,22 diuretics, nephrotoxic medications, corticosteroids, hypoglycemic medications, and narcotic analgesics), reconciliation of the discharge medication regimen with preadmission medications and designation of medications as new, modified, or discontinued,23 and emphasis on assessing patient understanding of medication self‐management plans.24 Several published studies found that pharmacist oversight of discharge medications or postdischarge telephone calls improved patient outcomes.1820 However, not every health system has the resources and infrastructure necessary to implement these types of programs. Moreover, methods of implementation of each of these discharge elements were believed to be beyond the scope of this project, so pharmacist involvement was not specifically included in this checklist.

The expert panel and workshop participants found items related to cognition and functional status to be important for patients whose usual cognitive or functional status was changed or whose status at discharge was not within normal limits.25, 26 Clinicians seeing patients in follow‐up would then have an important reference point for evaluating progress and the need for additional home support or therapy. Patients with limited literacy or language barriers may need these issues assessed with the help of family members and/or translators to identify changes from their baseline level of functioning.

In addition, resuscitation status was viewed by the group as an important data element for some patients,27 particularly those who had been critically ill. Development of disease or population‐specific content, for example, for patients with heart failure or pneumonia, was also identified as critical to the safe discharge of elderly patient, with the understanding that there may be a need to modify and individualize the content for patients with complex conditions and multiple comorbidities.

The content of the hospital discharge summary deemphasized the need for a complete history of the present illness at the time of hospital admission or an exhaustive hospital course. Instead, it highlighted the need to identify a patient's condition at discharge, pending issues and interventions requiring ongoing and focused monitoring, contingency planning, and contact information of knowledgeable providers in case questions arise after discharge.2830

Postdischarge care was emphasized with the need for a follow‐up appointment within at most 2 weeks of discharge or sooner for patients with fragile clinical conditions.31 Although this was not recommended because of a published study, it was the consensus of the expert panel and peer review process that close follow‐up after hospital discharge was critical in ensuring medication safety. Transportation limitations and other logistical problems with access to a follow‐up clinician were identified as important issues to be resolved in the discharge planning process in order for timely follow‐up to occur. In addition, it was deemed critical that the follow‐up provider receive the key information about the hospitalization with any necessary follow‐up instructions as soon after discharge as possible13 and certainly before the first postdischarge visit. Instructions to patients about medication schedules and follow‐up care need to be in writing at a 6th‐grade reading level; furthermore, processes to identify a patient's level of understanding of the follow‐up plan and areas for targeted education need to be established.24

DISCUSSION

We believe the development of a checklist of required elements to be communicated at discharge is a key step toward standardizing the hospital discharge process. The checklist highlights what is believed to be the key information about the transition of care and its process. The checklist is intended to standardize what is required for a successful hospital discharge. However, each institution will need to further refine this list according to local factors such as patient population, resources, and culture and to determine how best to implement the necessary changes to their current discharge process. Local modification of the checklist also allows for the addition of other elements that are patient‐ or population specific. Elderly patients discharged home from the hospital are the primary patient population targeted by this checklist ; there may be unique and additional elements necessary for an ideal discharge for a patient who is discharged to a subacute or acute rehabilitation facility. These elements are not described in this checklist but will be the focus of future work.

Establishing the critical elements of a hospital discharge transition sets the stage for improving patient outcomes in the immediate postdischarge period. Most important, the checklist conveys the message that the discharge process requires critical thinking, collaboration, and goal setting and that this coordination of care takes time. However, the discharge checklist must reside within a hospital culture that in general does not value the discharge process in the same way it values the admission process. The latter is more standardized and incorporates expectations about content and communication. In the same way, the current discharge is an admission to the next health care setting and deserves at least as much time and effort as a hospital admission. Furthermore, if institutions examine their current discharge processes, they may find that the time necessary to complete the discharge may be similar to the time necessary to admit a patient to the hospital. Finally, organizations need to develop internal policies and procedures that monitor and provide feedback about important dimensions of the discharge process, including content, patient understanding, information transfer, and clinical and service outcomes including satisfaction of the patient and the postdischarge provider. Hospital discharge is truly a team process involving nurses, pharmacists, case managers, and other hospital personnel, so performance measurement should be at the team or unit level, unlike other areas for which individual physicians may receive feedback on performance.

The limitations of the checklist development process include the paucity of randomized, controlled trials focused on the study of health care delivery processes and the lack of an industry gold standard. Furthermore, the heterogeneity of health care delivery systems makes it difficult to recommend specific interventions without understanding the myriad local issues. Those who provided input into this checklist included members of the inpatient team, a scope that can be broadened in the future to include outpatient physicians, patients, and caregivers in the home and long‐term care environments. However, the elements defined through the checklist serve as a starting point for developing discharge transition standards for older adults.

As leaders in hospital care, hospitalists are positioned to raise awareness of the importance of hospital discharge and to lead multidisciplinary efforts to improve the discharge process within their organizations. The first step in that process should be understanding the required elements and local facilitating factors and barriers in achieving a predictable, seamless transition of care for hospitalized patients.

Hospital discharge is a critical transition point for many inpatients. Patient recovery from diseases requiring hospitalization is frequently incomplete and requires ongoing management and evaluation after discharge. For hospitalists who focus their practice primarily on inpatient care, the handoff to the outpatient setting frequently involves a change in health care provider and care team. Changes in care environment and care goals can lead to adverse patient‐ and system‐level events.1 High‐risk patients with multiple medical issues and elderly patients are especially vulnerable to the consequences of ineffective discharge handoffs.2, 3

Several studies have identified the errors that commonly occur around the time of hospital discharge. Forster et al.4 found that 1 in 5 patients experiences an adverse event (defined as an injury resulting from medical management rather than from the underlying disease) in the transition from hospital to home. They also found that approximately 62% of adverse events could be either prevented or ameliorated.4 Roy et al. examined test results pending at the time of discharge and determined that posthospital providers were frequently unaware of pending test results, with a potentially serious clinical impact.5 In an analysis of adverse events at 2 large hospitals in the United Kingdom, Neale et al. found that almost 11% of those hospitalized had an adverse event, 18% of which were attributable to the discharge process.6

Communication of important transitional care issues to the posthospital care team and to the patient is essential to a safe transition. Studies by van Walraven et al. found that patient follow‐up with a physician who had access to the hospital discharge summary was associated with a decreased risk of rehospitalization.7 Patients not understanding discharge medications,8 dietary restrictions, or other lifestyle changes such as smoking cessation and exercise can lead to ineffective care transitions. Furthermore, the health system's barriers to effective patient self‐management may exacerbate the risk in the transition from the hospital setting.2, 913

In addition to the growing research literature that has identified gaps in the discharge process, the Joint Commission for the Accreditation of Healthcare Organizations (JCAHO) has included discharge instructions as a core performance measure in the care of heart failure patients. Hospital performance on this measure is reported publicly on the Centers for Medicare and Medicaid Services website (www.hospitalcompare.hhs.gov). Furthermore, the 2006 JCAHO patient safety goal of medication reconciliation recognizes the importance of preventing lapses in medication safety at points of care transition.14, 15 JCAHO now requires the development and implementation of processes to collect, review, reconcile, and document prescribed medications at all points of care transition, including hospital discharge.16

Older adults are considered more vulnerable to adverse events after discharge.8 They account for approximately 12% of the total U.S. population, but they make up 70% of hospitalized patients.17 With these factors in mind, the Society of Hospital Medicine (SHM) identified the elderly as a group especially vulnerable to the clinical care handoffs that occur in the hospital discharge process and therefore the patient population targeted in constructing the required elements of an ideal hospital discharge.

In addition to identifying a target patient population, inclusion of stakeholders primarily responsible for implementation is critical to developing a new process standard. In this instance, the hospitalist was identified as a critical architect of the development of the ideal discharge process, although clearly the hospitalist is just one of many people ultimately responsible for coordinating an effective hospital discharge. Finally, the organizations within which the elderly receive care and at which hospitalists practice are important partners in the implementation of systems of care that facilitate seamless care transitions.

In examining the myriad stakeholders involved in the discharge transitionthe patient, the hospitalist, other caregivers involved in hospital care, and the organizationSHM's Hospital Quality & Patient Safety (HQPS) Committee undertook an initiative to develop a practical list of important elements for hospitalists to include in the discharge of elderly inpatients, referred to in this article as the discharge checklist.

METHODS

In a process similar to that used by professional societies in the development of clinical guidelines, the SHM HQPS Committee used a combination of evidence‐based review and expert panels to develop a discharge checklist for elderly patients. Given that the focus of this project was a process improvement rather than a specific clinical condition, the SHM also believed it was critical to share the draft checklist with academic and community‐based practitioners knowledgeable in both the myriad logistical issues of and potential barriers to improving the discharge transition. The detailed process for checklist development is outlined below and summarized in Figure 1.

Figure 1
Process of development of the discharge checklist.

Literature Review

A Medline search was performed using the keywords patient discharge and either quality indicators, health care, or quality of health care. Articles included were those written in English and published between January 1975 and January 2005. We also reviewed the abstracts submitted to the SHM's 2003‐2005 annual and regional meetings in and reviewed those that included the designated keywords in their content focus. The number of articles selected was narrowed from 274 to 32 by including only studies of specific discharge elements, articles describing adverse events associated with but not including specific discharge elements, descriptions of tools to gather and report important data at the time of hospital discharge, or recommendations of experts or medical associations about methods of improving the discharge process.

DRAFT Checklist and Expert Review

Two members of the discharge checklist team (S.K. and D.M.) reviewed all 32 relevant reports and assembled a list of possible items for inclusion in an ideal hospital discharge. Inclusion of items was based on clinical relevance to elderly patients and impact on postdischarge care. This list initially contained 24 items in 3 domainsdischarge planning, medications, and the discharge summary document.

The list was sent to 3 experts, selected on the basis of their academic expertise in the fields of geriatrics and care transitions. Each independently reviewed the list, and then all 3 experts met several times by conference call. Items approved by at least 2 of the 3 experts were retained. The revised checklist transformed the 3 domains originally identified into 9 main elements, each with 2‐5 subelements.

Peer Review at SHM Annual Meeting

In a workshop at the 2005 SHM Annual Meeting, a facilitator presented the checklist and moderated a discussion among several experts from the task force and expert panel. The expert panel shared relevant background literature and key findings from their own research. Audience members included community and academic hospitalists, case managers, and pharmacists. Many attendees responded to the checklist and raised relevant issues. In all, 120 clinicians participated in this 90‐minute workshop.

After reviewing the checklist, workshop attendees gave both formal and informal input into the checklist content. Through group discussion and individual suggestions, items were added to the checklist. This process resulted in the addition of 1 main element and 3 subelements. At its completion, each workshop participant was allowed up to 3 votes for items that they believed should be removed from the modified checklist. The results were tallied, and the checklist was further reviewed and critiqued by the workshop faculty. Elements of the discharge checklist were designated as required for optimal handoffs if there was consensus among the committee members and workshop attendees. Elements that did not have unanimous support were discussed further and designated as optional. The final checklist was then developed with both required and optional elements and endorsed by the HQPS Committee and the SHM board.

RESULTS

The final discharge checklist is shown in Figure 2. It contains required and optional data elements and processes for 3 types of discharge documents: the discharge summary, patient instructions, and communication (by phone, e‐mail, or fax) on the day of discharge to the receiving provider. Other documents, such as transfer orders for a rehabilitation facility or nursing home, were considered outside the scope of this project.

Figure 2
Ideal discharge of the elderly patient: a hospitalist checklist. x = required element; o = optional element.

The literature review identified medications as a significant source of adverse events for patients upon hospital discharge.4, 8, 14, 1820 The expert panel and workshop participants all endorsed the need for additional detailed attention to reviewing and reconciling medications during the discharge process. The use of standardized tools was suggested by the group to improve the medication review process.21 The required elements include not only a list of discharge medications but also attention to high‐risk medications that require closer postdischarge follow‐up and monitoring (such as warfarin,22 diuretics, nephrotoxic medications, corticosteroids, hypoglycemic medications, and narcotic analgesics), reconciliation of the discharge medication regimen with preadmission medications and designation of medications as new, modified, or discontinued,23 and emphasis on assessing patient understanding of medication self‐management plans.24 Several published studies found that pharmacist oversight of discharge medications or postdischarge telephone calls improved patient outcomes.1820 However, not every health system has the resources and infrastructure necessary to implement these types of programs. Moreover, methods of implementation of each of these discharge elements were believed to be beyond the scope of this project, so pharmacist involvement was not specifically included in this checklist.

The expert panel and workshop participants found items related to cognition and functional status to be important for patients whose usual cognitive or functional status was changed or whose status at discharge was not within normal limits.25, 26 Clinicians seeing patients in follow‐up would then have an important reference point for evaluating progress and the need for additional home support or therapy. Patients with limited literacy or language barriers may need these issues assessed with the help of family members and/or translators to identify changes from their baseline level of functioning.

In addition, resuscitation status was viewed by the group as an important data element for some patients,27 particularly those who had been critically ill. Development of disease or population‐specific content, for example, for patients with heart failure or pneumonia, was also identified as critical to the safe discharge of elderly patient, with the understanding that there may be a need to modify and individualize the content for patients with complex conditions and multiple comorbidities.

The content of the hospital discharge summary deemphasized the need for a complete history of the present illness at the time of hospital admission or an exhaustive hospital course. Instead, it highlighted the need to identify a patient's condition at discharge, pending issues and interventions requiring ongoing and focused monitoring, contingency planning, and contact information of knowledgeable providers in case questions arise after discharge.2830

Postdischarge care was emphasized with the need for a follow‐up appointment within at most 2 weeks of discharge or sooner for patients with fragile clinical conditions.31 Although this was not recommended because of a published study, it was the consensus of the expert panel and peer review process that close follow‐up after hospital discharge was critical in ensuring medication safety. Transportation limitations and other logistical problems with access to a follow‐up clinician were identified as important issues to be resolved in the discharge planning process in order for timely follow‐up to occur. In addition, it was deemed critical that the follow‐up provider receive the key information about the hospitalization with any necessary follow‐up instructions as soon after discharge as possible13 and certainly before the first postdischarge visit. Instructions to patients about medication schedules and follow‐up care need to be in writing at a 6th‐grade reading level; furthermore, processes to identify a patient's level of understanding of the follow‐up plan and areas for targeted education need to be established.24

DISCUSSION

We believe the development of a checklist of required elements to be communicated at discharge is a key step toward standardizing the hospital discharge process. The checklist highlights what is believed to be the key information about the transition of care and its process. The checklist is intended to standardize what is required for a successful hospital discharge. However, each institution will need to further refine this list according to local factors such as patient population, resources, and culture and to determine how best to implement the necessary changes to their current discharge process. Local modification of the checklist also allows for the addition of other elements that are patient‐ or population specific. Elderly patients discharged home from the hospital are the primary patient population targeted by this checklist ; there may be unique and additional elements necessary for an ideal discharge for a patient who is discharged to a subacute or acute rehabilitation facility. These elements are not described in this checklist but will be the focus of future work.

Establishing the critical elements of a hospital discharge transition sets the stage for improving patient outcomes in the immediate postdischarge period. Most important, the checklist conveys the message that the discharge process requires critical thinking, collaboration, and goal setting and that this coordination of care takes time. However, the discharge checklist must reside within a hospital culture that in general does not value the discharge process in the same way it values the admission process. The latter is more standardized and incorporates expectations about content and communication. In the same way, the current discharge is an admission to the next health care setting and deserves at least as much time and effort as a hospital admission. Furthermore, if institutions examine their current discharge processes, they may find that the time necessary to complete the discharge may be similar to the time necessary to admit a patient to the hospital. Finally, organizations need to develop internal policies and procedures that monitor and provide feedback about important dimensions of the discharge process, including content, patient understanding, information transfer, and clinical and service outcomes including satisfaction of the patient and the postdischarge provider. Hospital discharge is truly a team process involving nurses, pharmacists, case managers, and other hospital personnel, so performance measurement should be at the team or unit level, unlike other areas for which individual physicians may receive feedback on performance.

The limitations of the checklist development process include the paucity of randomized, controlled trials focused on the study of health care delivery processes and the lack of an industry gold standard. Furthermore, the heterogeneity of health care delivery systems makes it difficult to recommend specific interventions without understanding the myriad local issues. Those who provided input into this checklist included members of the inpatient team, a scope that can be broadened in the future to include outpatient physicians, patients, and caregivers in the home and long‐term care environments. However, the elements defined through the checklist serve as a starting point for developing discharge transition standards for older adults.

As leaders in hospital care, hospitalists are positioned to raise awareness of the importance of hospital discharge and to lead multidisciplinary efforts to improve the discharge process within their organizations. The first step in that process should be understanding the required elements and local facilitating factors and barriers in achieving a predictable, seamless transition of care for hospitalized patients.

References
  1. Cook RI,Render M,Woods DD.Gaps in the continuity of care and progress on patient safety.BMJ.2000;320:791794.
  2. Bull MJ,Hansen HE,Gross CR.Predictors of elder and family caregiver satisfaction with discharge planning.J Cardiovasc Nurs.2000;14:7687.
  3. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders: a randomized clinical trial.JAMA.1999;281:613620.
  4. Forster AJ,Murff HJ,Peterson JF, et al.The incidence and severity of adverse events affecting patients after discharge from the hospital.Ann Intern Med.2003;138:161167.
  5. Roy C,Poon EG,Karson AS, et al.Patient safety concerns arising from test results that return after hospital discharge.Ann Intern Med.2005;143:121128.
  6. Neale G,Woloshynowych M,Vincent C.Exploring the causes of adverse events in NHS hospital practice.J. R. Soc Med.2001;94:553.
  7. van Walraven C,Seth R,Austin PC,Laupacis A.Effect of discharge summary availability during the post‐discharge visits on hospital readmission.J Gen Intern Med.2002;17:186192.
  8. Martens KH.An ethnographic study of the process of medication discharge education (MDE).J Adv Nurs.1998;27:341348.
  9. Cleary PD.A hospitalization from hell: a patient's perspective on quality.Ann Intern Med.2003;138:3339.
  10. Demlo LK,Campbell PM.Improving discharge data: lessons from the National Hospital Discharge Survey.Med Care1981;19:10301040.
  11. Felden JM,Scott S,Horne JG.An investigation of patient satisfaction following discharge after total hip replacement surgery.Orthop Nurs.2003;22:429436.
  12. Hickey ML,Kleefield SF,Pearson SD, et al.Payer‐hospital collaboration to improve patient satisfaction with hospital discharge.Jt Comm J QuaI Improv.1996;22:336344.
  13. van Walraven C,Mamdani M,Fang J,Austin PC.Continuity of care and patient outcomes after hospital discharge.J Gen Intern Med.2004;19:624631.
  14. Resar R.Will, ideas, and execution: their role in reducing adverse medication events.J Pediatr.2005;147:727728.
  15. Resar R.Why we need to learn standardisation.Aust Fam Physician.2005;34(1‐2):6768.
  16. Joint Commission on Accreditation of Healthcare Organizations.2006 Critical Access Hospital and Hospital National Patient Safety Goals. Available at: http://www.jcaho.org/accredited+organizations/patient+safety/06_npsg/06_npsg_cah_hap.htm.
  17. Census Bureau of Statistics,2000.
  18. Kucukarslan S,Peters M,Mlynarek , et al.Pharmacists on rounding teams reduce preventable adverse events in hospital general medicine units.Arch Intern Med.2003;163:20142018.
  19. Dudas V,Bookwalter T,Kerr K, et al.The impact of follow‐up telephone calls to patients after hospitalization.Ann Intern Med.2001;111(9B):26S30S.
  20. Schnipper JL,Kirwin JL,Cotugno MC, et al.Role of pharmacist counseling in preventing adverse drug events after hospitalization.Arch Intern Med.2006;166:565571.
  21. Lewis T.Using the NO TEARS tool for medication review.BMJ.2004;329:434.
  22. Manning DM.Toward safer warfarin therapy: does precise daily dosing improve INR control?Mayo Clinic Proc.2002;77:873875.
  23. Resar R.Institute for Healthcare Improvement, personal communication.
  24. Institute of Medicine.Kindig DA, editor.Health Literacy: A Prescription to End Confusion.Washington, DC:National Academies Press,2004.
  25. Manning DM,Keller AS,Frank DL.Independent Mobility Validation Exam (I‐MOVE): a tool for periodic reassessment of fall‐risk and discharge planning. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
  26. Mathias S,Nayak US,Isaacs B.Balance in elderly patients: the “get‐up‐and‐go” test.Arch Phys Med Rehabil.1986;67:387389.
  27. AMA, Council on Ethical and Judicial Affairs.Guidelines for appropriate use of “do‐not‐resuscitate” orders.JAMA.1991;265:18681871.
  28. van Walraven C,Weinberg AL.Quality assessment of a discharge summary system.CMAJ.1995;152:14371442.
  29. van Walraven C,Rokosh E.What is necessary for high‐quality discharge summaries?Am J Med Qual.1999.14:160169.
  30. JCAHO Manual: Information Management (IM) 6.10 and Patient Care (PC) 15.30
  31. Whitford K,Huddleston JM.Specific appointments after pneumonia hospitalization reduce readmissions. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
References
  1. Cook RI,Render M,Woods DD.Gaps in the continuity of care and progress on patient safety.BMJ.2000;320:791794.
  2. Bull MJ,Hansen HE,Gross CR.Predictors of elder and family caregiver satisfaction with discharge planning.J Cardiovasc Nurs.2000;14:7687.
  3. Naylor MD,Brooten D,Campbell R, et al.Comprehensive discharge planning and home follow‐up of hospitalized elders: a randomized clinical trial.JAMA.1999;281:613620.
  4. Forster AJ,Murff HJ,Peterson JF, et al.The incidence and severity of adverse events affecting patients after discharge from the hospital.Ann Intern Med.2003;138:161167.
  5. Roy C,Poon EG,Karson AS, et al.Patient safety concerns arising from test results that return after hospital discharge.Ann Intern Med.2005;143:121128.
  6. Neale G,Woloshynowych M,Vincent C.Exploring the causes of adverse events in NHS hospital practice.J. R. Soc Med.2001;94:553.
  7. van Walraven C,Seth R,Austin PC,Laupacis A.Effect of discharge summary availability during the post‐discharge visits on hospital readmission.J Gen Intern Med.2002;17:186192.
  8. Martens KH.An ethnographic study of the process of medication discharge education (MDE).J Adv Nurs.1998;27:341348.
  9. Cleary PD.A hospitalization from hell: a patient's perspective on quality.Ann Intern Med.2003;138:3339.
  10. Demlo LK,Campbell PM.Improving discharge data: lessons from the National Hospital Discharge Survey.Med Care1981;19:10301040.
  11. Felden JM,Scott S,Horne JG.An investigation of patient satisfaction following discharge after total hip replacement surgery.Orthop Nurs.2003;22:429436.
  12. Hickey ML,Kleefield SF,Pearson SD, et al.Payer‐hospital collaboration to improve patient satisfaction with hospital discharge.Jt Comm J QuaI Improv.1996;22:336344.
  13. van Walraven C,Mamdani M,Fang J,Austin PC.Continuity of care and patient outcomes after hospital discharge.J Gen Intern Med.2004;19:624631.
  14. Resar R.Will, ideas, and execution: their role in reducing adverse medication events.J Pediatr.2005;147:727728.
  15. Resar R.Why we need to learn standardisation.Aust Fam Physician.2005;34(1‐2):6768.
  16. Joint Commission on Accreditation of Healthcare Organizations.2006 Critical Access Hospital and Hospital National Patient Safety Goals. Available at: http://www.jcaho.org/accredited+organizations/patient+safety/06_npsg/06_npsg_cah_hap.htm.
  17. Census Bureau of Statistics,2000.
  18. Kucukarslan S,Peters M,Mlynarek , et al.Pharmacists on rounding teams reduce preventable adverse events in hospital general medicine units.Arch Intern Med.2003;163:20142018.
  19. Dudas V,Bookwalter T,Kerr K, et al.The impact of follow‐up telephone calls to patients after hospitalization.Ann Intern Med.2001;111(9B):26S30S.
  20. Schnipper JL,Kirwin JL,Cotugno MC, et al.Role of pharmacist counseling in preventing adverse drug events after hospitalization.Arch Intern Med.2006;166:565571.
  21. Lewis T.Using the NO TEARS tool for medication review.BMJ.2004;329:434.
  22. Manning DM.Toward safer warfarin therapy: does precise daily dosing improve INR control?Mayo Clinic Proc.2002;77:873875.
  23. Resar R.Institute for Healthcare Improvement, personal communication.
  24. Institute of Medicine.Kindig DA, editor.Health Literacy: A Prescription to End Confusion.Washington, DC:National Academies Press,2004.
  25. Manning DM,Keller AS,Frank DL.Independent Mobility Validation Exam (I‐MOVE): a tool for periodic reassessment of fall‐risk and discharge planning. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
  26. Mathias S,Nayak US,Isaacs B.Balance in elderly patients: the “get‐up‐and‐go” test.Arch Phys Med Rehabil.1986;67:387389.
  27. AMA, Council on Ethical and Judicial Affairs.Guidelines for appropriate use of “do‐not‐resuscitate” orders.JAMA.1991;265:18681871.
  28. van Walraven C,Weinberg AL.Quality assessment of a discharge summary system.CMAJ.1995;152:14371442.
  29. van Walraven C,Rokosh E.What is necessary for high‐quality discharge summaries?Am J Med Qual.1999.14:160169.
  30. JCAHO Manual: Information Management (IM) 6.10 and Patient Care (PC) 15.30
  31. Whitford K,Huddleston JM.Specific appointments after pneumonia hospitalization reduce readmissions. Abstract and Poster presentation at SHM (formerly NAIP) 5th Annual Meeting, Philadelphia, PA, April 9,2002.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
354-360
Page Number
354-360
Article Type
Display Headline
Transition of care for hospitalized elderly patients—Development of a discharge checklist for hospitalists
Display Headline
Transition of care for hospitalized elderly patients—Development of a discharge checklist for hospitalists
Legacy Keywords
care standardization, continuity of care transition and discharge planning, multidisciplinary care
Legacy Keywords
care standardization, continuity of care transition and discharge planning, multidisciplinary care
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
Associate Chair, Department of Internal Medicine, 5333 McAuley Drive, RHB 5112, Ypsilanti, MI 48197
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Pneumonia: 3 days of antibiotics for uncomplicated course

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
Pneumonia: 3 days of antibiotics for uncomplicated course

  • CLINICAL QUESTION: In patients hospitalized for treatment of community‐acquired pneumonia, can treatment be stopped after 3 days if the patient has substantially improved?

  • BOTTOM LINE: Dogma successfully challenged: In patients who respond well to initial treatment, stopping antibiotic therapy after 3 days is just as effective as continuing treatment for the standard 8 days. (LOE = 1b)

  • REFERENCE: el Moussaoui R, de Borgie CA, van den Broek P, et al. Effectiveness of discontinuing antibiotic treatment after three days versus eight days in mild to moderatesevere community acquired pneumonia: randomised, double blind study. BMJ 2006;332:13551358.

  • STUDY DESIGN: Randomized controlled trial (doubleblinded)

  • FUNDING: Industry

  • ALLOCATION: Uncertain

  • SETTING: Inpatient (any location)

  • SYNOPSIS: The treatment of pneumonia for 7 days to 10 days is based on tradition, not scientific evidence. The researchers conducting this study challenged the status quo by enrolling 119 adults with mild to moderatesevere communityacquired pneumonia with a severity index score of 110 or less. On admission, all patients were started on intravenous amoxicillin, the preferred empirical treatment in the Netherlands. After 72 hours of treatment, patients who showed improvement in symptoms, had a temperature of less than 38 C, and could take oral drugs were randomized to treatment with placebo or amoxicillin 750 mg 3 times daily for 5 days. Using modified intentiontotreat analysis, after 10 days 89% of patients in both groups were clinically cured. In followup at 28 days, clinical cure rates were also similar between the 2 approaches, as was bacteriologic success and radiologic success. This study was designed to find a difference in success rates of at least 10%. There are a couple of notable limitations to this study. First, the patients in the shorttreatment group had a median age of 54 years compared with 60 years in the 8day group, and these younger patients may be more likely to respond to the short course, thus skewing the results. Second, the study was conducted in the Netherlands, where resistance patterns may be different than in other countries. Finally, the study was conducted in 9 hospitals over 3 years, which works out to less than 5 patients per hospital per year recruited into the study. Given the imbalance in age and this sparse representation, these patients could be highly selected and not representative of the typical patient admitted to a community hospital.

Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
387-387
Sections
Article PDF
Article PDF

  • CLINICAL QUESTION: In patients hospitalized for treatment of community‐acquired pneumonia, can treatment be stopped after 3 days if the patient has substantially improved?

  • BOTTOM LINE: Dogma successfully challenged: In patients who respond well to initial treatment, stopping antibiotic therapy after 3 days is just as effective as continuing treatment for the standard 8 days. (LOE = 1b)

  • REFERENCE: el Moussaoui R, de Borgie CA, van den Broek P, et al. Effectiveness of discontinuing antibiotic treatment after three days versus eight days in mild to moderatesevere community acquired pneumonia: randomised, double blind study. BMJ 2006;332:13551358.

  • STUDY DESIGN: Randomized controlled trial (doubleblinded)

  • FUNDING: Industry

  • ALLOCATION: Uncertain

  • SETTING: Inpatient (any location)

  • SYNOPSIS: The treatment of pneumonia for 7 days to 10 days is based on tradition, not scientific evidence. The researchers conducting this study challenged the status quo by enrolling 119 adults with mild to moderatesevere communityacquired pneumonia with a severity index score of 110 or less. On admission, all patients were started on intravenous amoxicillin, the preferred empirical treatment in the Netherlands. After 72 hours of treatment, patients who showed improvement in symptoms, had a temperature of less than 38 C, and could take oral drugs were randomized to treatment with placebo or amoxicillin 750 mg 3 times daily for 5 days. Using modified intentiontotreat analysis, after 10 days 89% of patients in both groups were clinically cured. In followup at 28 days, clinical cure rates were also similar between the 2 approaches, as was bacteriologic success and radiologic success. This study was designed to find a difference in success rates of at least 10%. There are a couple of notable limitations to this study. First, the patients in the shorttreatment group had a median age of 54 years compared with 60 years in the 8day group, and these younger patients may be more likely to respond to the short course, thus skewing the results. Second, the study was conducted in the Netherlands, where resistance patterns may be different than in other countries. Finally, the study was conducted in 9 hospitals over 3 years, which works out to less than 5 patients per hospital per year recruited into the study. Given the imbalance in age and this sparse representation, these patients could be highly selected and not representative of the typical patient admitted to a community hospital.

  • CLINICAL QUESTION: In patients hospitalized for treatment of community‐acquired pneumonia, can treatment be stopped after 3 days if the patient has substantially improved?

  • BOTTOM LINE: Dogma successfully challenged: In patients who respond well to initial treatment, stopping antibiotic therapy after 3 days is just as effective as continuing treatment for the standard 8 days. (LOE = 1b)

  • REFERENCE: el Moussaoui R, de Borgie CA, van den Broek P, et al. Effectiveness of discontinuing antibiotic treatment after three days versus eight days in mild to moderatesevere community acquired pneumonia: randomised, double blind study. BMJ 2006;332:13551358.

  • STUDY DESIGN: Randomized controlled trial (doubleblinded)

  • FUNDING: Industry

  • ALLOCATION: Uncertain

  • SETTING: Inpatient (any location)

  • SYNOPSIS: The treatment of pneumonia for 7 days to 10 days is based on tradition, not scientific evidence. The researchers conducting this study challenged the status quo by enrolling 119 adults with mild to moderatesevere communityacquired pneumonia with a severity index score of 110 or less. On admission, all patients were started on intravenous amoxicillin, the preferred empirical treatment in the Netherlands. After 72 hours of treatment, patients who showed improvement in symptoms, had a temperature of less than 38 C, and could take oral drugs were randomized to treatment with placebo or amoxicillin 750 mg 3 times daily for 5 days. Using modified intentiontotreat analysis, after 10 days 89% of patients in both groups were clinically cured. In followup at 28 days, clinical cure rates were also similar between the 2 approaches, as was bacteriologic success and radiologic success. This study was designed to find a difference in success rates of at least 10%. There are a couple of notable limitations to this study. First, the patients in the shorttreatment group had a median age of 54 years compared with 60 years in the 8day group, and these younger patients may be more likely to respond to the short course, thus skewing the results. Second, the study was conducted in the Netherlands, where resistance patterns may be different than in other countries. Finally, the study was conducted in 9 hospitals over 3 years, which works out to less than 5 patients per hospital per year recruited into the study. Given the imbalance in age and this sparse representation, these patients could be highly selected and not representative of the typical patient admitted to a community hospital.

Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
387-387
Page Number
387-387
Article Type
Display Headline
Pneumonia: 3 days of antibiotics for uncomplicated course
Display Headline
Pneumonia: 3 days of antibiotics for uncomplicated course
Sections
Article Source
Copyright © 2006 by Wiley Subscription Services, Inc.
Disallow All Ads
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Improved Prophylaxis Following Education

Article Type
Changed
Sun, 05/28/2017 - 22:45
Display Headline
Improved use of thromboprophylaxis for deep vein thrombosis following an educational intervention

Venous thromboembolism (VTE), which encompasses both deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of the morbidity and mortality of hospitalized medical patients.1 Hospitalization for an acute medical illness has been associated with an 8‐fold increase in the relative risk of VTE and is responsible for approximately a quarter of all VTE cases in the general population.2, 3

Current evidence‐based guidelines, including those from the American College of Chest Physicians (ACCP), recommend prophylaxis with low‐dose unfractionated heparin (UFH) or low‐molecular‐weight heparin (LMWH) for medical patients with risk factors for VTE.4, 5 Mechanical prophylaxis methods including graduated compression stockings and intermittent pneumatic compression are recommended for those patients for whom anticoagulant therapy is contraindicated because of a high risk of bleeding.4, 5 However, several studies have shown that adherence to these guidelines is suboptimal, with many at‐risk patients receiving inadequate prophylaxis (range 32%‐87%).610

Physician‐related factors identified as potential barriers to guideline adherence include not being aware or familiar with the guidelines, not agreeing with the guidelines, or believing the guideline recommendations to be ineffective.11 More specific studies have shown that some physicians may lack basic knowledge regarding the current treatment standards for VTE and may underestimate the significance of VTE.1213 As distinct strategies, education aimed at disseminating VTE prophylaxis guidelines, as well as regular audit‐and‐feedback of physician performance, has been shown to improve rates of VTE prophylaxis in clinical practice.6, 1417 Implementation of educational programs significantly increased the level of appropriate VTE prophylaxis from 59% to 70% of patients in an Australian hospital15 and from 73% to 97% of patients in a Scottish hospital.14 Another strategy, the use of point‐of‐care electronically provided reminders with decision support, has been successful not only in increasing the rates of VTE prophylaxis, but also in decreasing the incidence of clinical VTE events.16 Although highly effective, electronic alerts with computerized decision support do not exist in many hospitals, and other methods of intervention are needed.

In this study, we evaluated adherence to the 2001 ACCP guidelines for VTE prophylaxis among medical patients in our teaching hospital. (The guidelines were updated in 2004, after our study was completed.) After determining that our baseline rates of appropriate VTE prophylaxis were suboptimal, we developed, implemented, and evaluated a multifaceted strategy to improve the rates of appropriate thromboprophylaxis among our medical inpatients.

Six categories of quality improvement strategies have been described: provider education, decision support, audit‐and‐feedback, patient education, organization change, and regulation and policy.18 The intervention we developed was a composite of 3 of these: provider education, decision support, and audit‐and‐feedback.

METHODS

Study Design and Patients

This was a before‐and‐after study designed to assess whether implementation of a VTE prophylaxis quality improvement intervention could improve the rate of appropriate thromboprophylaxis in hospitalized medical patients at the State University of New York, Downstate Medical CenterUniversity Hospital of Brooklyn, an urban university teaching hospital of approximately 400 beds. This initiative, conducted as part of a departmental quality assurance and performance improvement program, did not require institutional review board approval. After an informal survey revealed a prophylaxis rate of approximately 50%, a more formal baseline assessment of the rate of medical patients receiving VTE prophylaxis was conducted during October 2002. This assessment was a single sampling of all medical inpatients on 2 of the medical floors on a single day. The results were consistent with those of the informal survey as well as those from an international registry.19 The results from the baseline study indicated that VTE prophylaxis was underused: only 46.9% of our medical inpatients received any form of prophylaxis. The prophylaxis rate was assessed again in 2 sampling periods beginning 12 and 18 months after implementation of the intervention. Data were collected monthly and combined into 3‐month blocks. The first postintervention sample (n = 116 patient charts) was drawn from a period 12‐14 months after implementation and the second (n = 147 patient charts) from a period 18‐20 months after implementation.

On a randomly designated day in the latter half of each month during each sampling period, all charts on 2 primary medical floors were reviewed and included in the retrospective analysis. Patients who were not on the medical service were excluded from analysis. Patients, as well as their medications, were identified using a list generated from our pharmacy database. We chose this method and schedule for several reasons. First, we sought to reduce the likelihood of including a patient more than once in a monthly sample. Second, by waiting for the latter half of the month we sought to allow house staff a chance to acquire knowledge from the educational program introduced on the first day of the month. Third, we wanted to allow house staff the time to actualize new attitudes reinforced by the audit‐and‐feedback element. The house staff included approximately 4 interns and 4 residents each month plus 10‐15 attendings or hospitalists.

Data Collection

For each sampling period we conducted a medical record (paper) review, and the Division Chief of General Internal Medicine also interviewed the medical house staff and attending physicians. Data collected included risk factors for VTE, contraindications to anticoagulant prophylaxis, type of VTE prophylaxis received, and appropriateness of the prophylaxis. Prophylaxis was considered appropriate when it was given in accordance with a risk stratification scheme (Table 1) adapted from the 2001 ACCP guideline recommendations for surgical patients20 and modified for medical inpatients, similar to the risk assessment model by Caprini et al.21 Prophylaxis was also considered appropriate when no prophylaxis was given for low‐risk patients or when full anticoagulation was given for another indication (Table 1). Questionable prophylaxis was defined as UFH given every 12 hours to a high‐risk patient. All other prophylaxis was deemed inappropriate (including no prophylaxis if prophylaxis was indicated, use of enoxaparin at incorrect prophylactic doses such as 60 or 20 mg, IPC alone for a high‐risk patient with no contraindication to pharmacological prophylaxis, and the use of warfarin if no other indication for it). The risk factors for thromboembolism and contraindications to anticoagulant prophylaxis are given in Table 2. Non‐ambulatory was defined as an order for bed rest with or without bathroom privileges or was judged based on information obtained from the medical house staff and nurses about whether the patient was ambulatory or had been observed walking outside his or her room. Data on pharmacological prophylaxis were obtained from the hospital pharmacy. Information on use of mechanical prophylaxis was obtained by house staff interviews or review of the order sheet. The house officer or attending physician of each patient was interviewed retrospectively to determine the reason for admission and the risk factors for VTE present on admission. Patients were classified as having low, moderate, high, or highest risk for VTE based on their age and any major risk factors for VTE (Table 1).19 All collected data were reported to the Department of Medicine Performance Improvement Committee for independent corroboration.

VTE Risk Categories and Appropriate Prophylaxisa
Risk categoryDefinitionDosage of appropriate prophylaxis
Age (years)Additional risk factorsbLow‐dose unfractionated heparinLMWH
  • Appropriate prophylaxis was defined as prophylaxis in accordance with the risk stratification scheme above, which was adopted from the ACCP 2001 guideline recommendations for surgical patients19 and modified for medically ill patients; appropriate prophylaxis also included no prophylaxis for low‐risk patients or patients on full anticoagulation (with warfarin, IV UFH, or LMWH) for other indications.

  • See Table 2.

  • CVA, cerebrovascular accident; LMWH, low‐molecular‐weight heparin; q12h, every 12 hours; q8h, every 8 hours; IPC, intermittent pneumatic compression; VTE, venous thromboembolism.

Low (0‐1 risk factors)<400‐1 factorNoneNone
Moderate (2 risk factors)40‐601 factor5000 units q12h40 mg of enoxaparin or 5000 units of dalteparin
High (3‐4 risk factors)>601‐2 factors or hypercoagulable state5000 units q8h or q12h (q8h recommended for surgical patients)40 mg of enoxaparin or 5000 units of dalteparin
Highest (5 or more factors)>40Malignancy, prior VTE, or CVA5000 units q8h plus IPCenoxaparin or dalteparin plus IPC
Risk Factors for Thromboembolism and Contraindications to Anticoagulant Prophylaxis
Risk factors for thromboembolism
Contraindications to anticoagulant prophylaxis
Age > 40 years
Infection
Inflammatory disease
Congestive heart failure
Chronic obstructive pulmonary disease
Prior venous thromboembolism
Cancer
Cerebrovascular accident
End‐stage renal disease
Hypercoagulable state
Atrial fibrillation
Recent surgery
Obesity
Non‐ambulatory
Active gastrointestinal bleed
Central nervous system bleed
Thrombocytopenia (platelet count <100,000/L)

Intervention Strategies

The intervention introduced comprised 3 strategies designed to improve VTE prophylaxis: provider education, decision support, and audit‐and‐feedback.

Provider Education

On the first day of every month, an orientation was given to all incoming medicine house staff by the chief resident that included information on the scope, risk factors, and asymptomatic nature of VTE, the importance of risk stratification, the need to provide adequate prophylaxis, and recommended prophylaxis regimens. A nurse educator also provided information to the nursing staff with the expectation that they would remind physicians to prescribe prophylactic treatment if not ordered initially; however, according to the nurses and house staff, this rarely occurred. Large posters showing VTE risk factors and prophylaxis were displayed at 2 nursing stations and physician charting rooms but were not visible to patients.

Decision Support

Pocket cards containing information on VTE risk factors and prophylaxis options were handed out to the house staff at the beginning of each month. These portable decision support tools assisted physicians in the selection of prophylaxis (a more recent, revised version of the material contained in this pocket guide is available at http://www.lovenox.com/hcp/dvtProphylaxisAndTreatment/dvtMedicalProphylaxis/guidelines.aspx#chart).

Audit‐and‐Feedback

Monthly audits were performed by the Division Chief of General Internal Medicine in order to evaluate the type and appropriateness of VTE prophylaxis prescribed (Table 3). During the orientation at the beginning of the month, the chief resident mentioned that an audit would take place sometime during the rotation. This random audit took place during the last 2 weeks of each month on the same day the data were requested from the pharmacy. Over 1‐2 days, physicians were interviewed either one to one or in a group, depending on the availability of house staff. All house staff and hospitalists were queried about the reasons for admission and the presence of VTE risk factors; physicians received feedback from the Division Chief on VTE risk category, prophylaxis, and appropriateness of prophylaxis treatment of their patients.

Educational Program
ElementTime/effort required
  • VTE, venous thromboembolism.

Orientation about VTE risk factors and the need to provide adequate prophylaxis given to all incoming house staff by the chief resident on the first day of every month10 min/month
Introduction of pocket cards containing information on VTE risk factors and prophylaxis options5 min/month
In‐hospital education of nurses by the nurse educator2 sessions of 1 h
Large posters presenting VTE risk factors and prophylaxis displayed in nursing stations and physician charting rooms5 min one time only
Monthly audits by the Division Chief of General Internal Medicine to evaluate the type and suitability of VTE prophylaxis prescribed2 h/month for interviews 2 h/month for record review/ data entry

Statistical Analysis

Differences in pre‐ and post‐intervention VTE prophylaxis and appropriate VTE prophylaxis rates were analyzed using the chi‐square test for categorical variables and the one‐way analysis of variance test for continuous variables. Differences were considered significant at the 5% level (P = .05).

RESULTS

Patients and Demographics

From October 2002 to August 2004 data were collected from 312 hospitalized medical patients: 49 patients in the baseline group during October 2002, and 116 and 147 at the 12‐ to 14‐month and 18‐ to 20‐month time points, respectively. Thus, approximately 40‐50 patients were randomly selected each month, representing 40% of the general medical service census. Patient demographics were similar between groups (Table 4). Overall, most patients were female (65.7%), and mean age was 61.2 years. The most common admission diagnoses were infection/sepsis (29.5%), chest pain/acute coronary syndromes/myocardial infarction (15.7%), heart failure (10.9%), and malignancy (9.6%). Overall, 7.1% (22 patients) had a contraindication to anticoagulant prophylaxis. The most common contraindication was active gastrointestinal bleeding on the current admission, which occurred in 18 of these patients.

Patient Demographics and Proportion of Patients with Risk Factors for Thrombosis in Each Study Group
 Baseline (n = 49)12 months (n = 116)18 months (n = 147)P valuea
  • P value determined using 3‐way chi‐square test unless otherwise stated.

  • P value determined using 3‐way ANOVA.

  • Due to missing data, n = 49, 82, and 140 in the baseline, 12‐month, and 18‐month groups, respectively.

  • Significantly different from baseline, P = .02. CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

Patient demographic
Mean age, years (SE)59.3 (2.6)63.3 (1.6)60.1 (1.5).25b
Men, n (%)20 (40.8)31 (26.7)56 (38.1).08
Contraindications to pharmacological prophylaxis, n (%)7 (14.3)5 (4.3)10 (6.8).07
Gastrointestinal bleeding5 (10.2)5 (4.3)8 (5.4) 
CNS bleeding1 (2.0)0 (0.0)0 (0.0) 
Low platelet count1 (2.0)0 (0.0)2 (1.4) 
Risk factor
Mean number of risk factors (SE)3.1 (0.2)2.7 (0.1)3.0 (0.1).05b
Non‐ambulatoryc46 (93.9)73 (89.0)112 (80.0)d.03
Age > 40 years39 (79.6)101 (87.1)122 (83.0).44
Cancer14 (28.6)15 (12.9)24 (16.3).05
End‐stage renal disease13 (26.5)29 (25.0)36 (24.5).96
Congestive heart failure11 (22.4)23 (19.8)28 (19.0).87
Infection8 (16.3)24 (20.7)46 (31.3).04
Cerebrovascular accident8 (16.3)12 (10.3)15 (10.2).47
COPD5 (10.2)9 (7.8)14 (9.5).84
Sepsis3 (6.1)6 (5.2)21 (14.3).03
Atrial fibrillation3 (6.1)8 (6.9)15 (10.2).52
Surgery1 (2.0)1 (0.9)2 (1.4).82
Previous venous thromboembolism0 (0.0)6 (5.2)8 (5.4).25
Obesity (morbid)0 (0.0)2 (1.7)2 (1.4).66
Hypercoagulable state0 (0.0)0 (0.0)0 (0.0) 

Risk Factors for VTE

Patient risk factors for VTE in each data collection period are summarized in Table 4. Analysis of this data showed that the most prevalent risk factors for VTE in the 3 patient populations were age older than 40 years (262/312, 84.0% of the total patient population) and nonambulatory state (231/271, 85.2% of the total population). Overall, the average number of risk factors for VTE was approximately 3, with more than 60% of patients having 3 or more VTE risk factors (Fig. 1).

Figure 1
Distribution of number of risk factors for venous thromboembolism.

Prophylaxis Use

The types of VTE prophylaxis used and the proportion of patients treated appropriately are summarized for each data collection period in Tables 5 and 6, respectively. In all 3 populations, most patients received pharmacological rather than mechanical prophylaxis, most commonly UFH. At baseline, the prophylaxis decision was appropriate (in accordance with the recommendations of the ACCP guidelines) as often as it was inappropriate (42.9% of patients). The prophylaxis decision was questionable in the remaining 14.3% of patients.

Summary of Prophylaxis Use in Each Patient Population
Prophylaxis typeBaseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using chi‐square test compared with baseline.

  • Full‐dose intravenous anticoagulation.

  • 5000 units subcutaneously.

  • qd, Once daily; bid, twice daily; tid, 3 times daily; UFH, unfractionated heparin; LWMH, low‐molecular‐weight heparin.

Any pharmacological22 (44.9)94 (81.0)<.01118 (80.3)<.01
Any UFH17 (34.7)61 (52.6).0458 (39.5).55
IV UFHb3 (6.1)5 (4.3) 2 (1.4) 
bid UFHc13 (26.5)43 (37.1) 39 (26.5) 
tid UFHc1 (2.0)10 (8.6) 16 (10.9) 
qd UFHc0 (0.0)3 (2.6) 1 (0.7) 
Any LMWH6 (12.2)30 (25.9).0559 (40.1)<.01
Mechanical prophylaxis1 (2.0)7 (6.0).2810 (6.8).21
Warfarin6 (12.2)20 (17.2).4219 (12.9).90
Summary of Appropriate Prophylaxis Use in Each Population
 Baseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using the chi‐square test compared with baseline.

  • LWMH, low‐molecular‐weight heparin; UFH, unfractionated heparin.

Receiving prophylaxis23 (46.9)100 (86.2)<.01127 (86.4)<.01
Appropriate21 (42.9)79 (68.1)<.01125 (85.0)<.01
UFH10 (20.4)33 (28.4).2845 (30.6).16
LMWH5 (10.2)27 (23.3).0558 (39.5)<.01
Questionable7 (14.3)28 (24.1).1414 (9.5).35
Inappropriate21 (42.9)9 (7.8)<.018 (5.4)<.01

Change in Prophylaxis Use

Twelve and 18 months after implementation of the quality improvement program, we observed an increase in the use of any prophylaxis, from 46.9% at baseline to 86.2% and 86.4%, respectively (Table 5; P < .01 in both groups versus baseline). This increase was a result almost entirely of an increase in the proportion of patients receiving pharmacological prophylaxis, which significantly increased, from 44.9% to 81.0% and 80.3%, at the 12‐ and 18‐month time points, respectively (Table 5; P < .01 for both groups versus baseline). Most meaningfully, there was a significant increase in the proportion of patients for whom an appropriate prophylaxis decision was made (from 42.9% to 68.1% and 85.0%, at the 12‐ and 18‐month time points, respectively; Table 6; P < .01 for both groups versus baseline). This represented a trend toward continuing increases in the use of appropriate prophylaxis as the study progressed (Fig. 2). This change was driven mainly by a significant increase in the prescribing of LMWH, almost all of which was prescribed in accordance with the 2001 ACCP guidelines (Table 6).

Figure 2
Run chart of appropriate prophylaxis rates.

DISCUSSION

In this study we evaluated the effect of an intervention that combined physician education with a decision support tool and a mechanism for audit‐and‐feedback. We have shown that implementation of such a multifaceted intervention is practical in a teaching hospital and can improve the rates of VTE prophylaxis use in medical patients. In nearly doubling the rate of appropriate prophylaxis, the effect size of our intervention was large, statistically significant, and sustained 18 months after implementation.

More than 60% of our patients had 3 or more risk factors, and more than 80% had at least 2 risk factors. The rate we observed for patients with 3 or more risk factors was 3 times higher than that reported previously.22 Despite the prevalence of high‐risk patients in our study, we observed that the preintervention rate of VTE prophylaxis among medical patients was relatively low at 47%, and only 43% of patients received prophylaxis in accordance with the ACCP guidelines. Our study findings are consistent with those of several other studies that have shown low rates of VTE prophylaxis in medical patients.6, 8, 2324 In a study of 15 hospitals in Massachusetts, only 13%‐19% of medical patients with indications and risk factors for VTE prophylaxis received any prophylaxis prior to an educational intervention.6 Similarly, a study of 368 consecutive medical patients at a Swiss hospital showed that only 22% of those at‐risk received VTE prophylaxis in accordance with the Thromboembolic Risk Factors (THRIFT) I Consensus Group recommendations.8 Results from 2 prospective patient registries also indicated low rates of VTE prophylaxis in medical patients.19, 24 In the IMPROVE registry of acutely ill medical patients, only 39% of patients hospitalized for 3 or more days received VTE prophylaxis19 and in the DVT‐FREE registry only 42% of medical patients with the inpatient diagnosis of DVT had received prophylaxis within 30 days of that diagnosis.24 In a recent retrospective study of 217 medical patients at the University of Utah hospital, just 43% of patients at high risk for VTE received any sort of prophylaxis.23

Physician education was the main intervention in several previous studies aimed at raising rates of VTE prophylaxis. Our study joins those that have also shown significant improvements after implementation of VTE prophylaxis educational initiatives.6, 14, 15, 23 In the study by Anderson et al., a significantly greater increase in the proportion of high‐risk patients receiving effective VTE prophylaxis was seen between 1986 and 1989 in hospitals that participated in a formal continuing medical education program compared with those that did not (increase: 28% versus 11%; P < .001).6 In 3 additional studies, educational interventions were shown to increase the rate of appropriate prophylaxis in at‐risk patients from 59% to 70%, from 55% to 96%, and from 43% to 72%.14, 15, 23

Other studies have cast doubt on the ability of time‐limited educational interventions to achieve a large or sustained effect.27, 28 A recent systematic review of strategies to improve the use of prophylaxis in hospitals concluded that a number of active strategies are likely to achieve optimal outcomes by combining a system for reminding clinicians to assess patients for VTE with assisting the selection of prophylaxis and providing audit‐and‐feedback.29 The large, sustained effect reported in our study might have been a result of the multifaceted and ongoing nature of the intervention, with reintroduction of the material to all incoming house staff each month. An audit from the last quarter of 2005nearly 2 years after the start of our interventionshowed that prophylaxis rates were approaching 100% (data not included in this study).

Another strategy, the use of computerized reminders to physicians, has been shown to increase the rate of VTE prophylaxis in surgical and medical/surgical patients.16, 26 Kucher et al. compared the incidence of DVT or PE in 1255 hospitalized patients whose physicians received an electronic alert of patient risk of DVT with 1251 hospitalized patients whose physicians did not receive such an alert. They found that the computer alert was associated with a significant reduction in the incidence of DVT or PE at 90 days, with a hazard ratio of 0.59 (95% confidence interval: 0.43, 0.81).16 Our study offers one practical alternative for those institutions that, like ours, do not currently have computerized order entry.

We were unable to determine if there was a specific element of the multifaceted VTE prophylaxis intervention program that contributed the most to the improvement in prophylaxis rates. Provider education was ongoing rather than just a single educational campaign. It was further supported by the pocket cards that provided support for decision making on VTE risk factors, risk categories (based on number and type of risk factor), recommended prophylaxis choices, and potential contraindications. In addition, our method of audit‐and‐feedback constructively leveraged the Hawthorne effect: aware that individual behavior was being measured, our physicians likely adjusted their practice accordingly. Taken together, it is likely that the several elements of our intervention were more powerful in combination than they would have been alone.

Although the multifaceted intervention worked well within our urban university teaching hospital, its application and outcome might be different for other types of hospitals. In our audit‐and‐feedback, for instance, review of resident physician performance was conducted by the Division Chief of General Internal Medicine, tapping into a very strong authority gradient. Hierarchical structures are likely to be different in other types of hospitals. It would therefore be valuable to examine whether the audit‐and‐feedback methodology presented in this article can be replicated in other hospital settings.

A potential limitation of this study was the use of retrospective review to determine baseline rates of VTE prophylaxis. This approach relies on medical notes being accurate and complete; such notes may not have been available for each patient. However, random reviews of both patient charts and hospital billing data for comorbidities performed after coding as a quality control step allowed for confirmation of the data or the extraction and addition of missing data. In addition, data collection was limited to a single day in the latter half of the month. It is not clear whether this sampling strategy collects data that are reflective of performance for the entire month. Our study was also limited by the absence of a control group. Without a control group, we cannot exclude the possibility that during the study factors other than the educational intervention might have contributed to the improvement in prophylaxis rates.

In this study we did not address whether an increase in VTE prophylaxis use translates to an improvement in patient outcomes, namely, a reduction in the rate of VTE. Mosen et al. showed that increasing the VTE prophylaxis rate by implementing a computerized reminder system did not decrease the rate of VTE.26 However, the baseline rate of VTE prophylaxis was already very good, and the study was only powered to detect a large difference in VTE rates. Conversely, Kucher et al. recently demonstrated a significant reduction in VTE events 90 days after initiation of a computerized alert program.16 Further studies designed to confirm the inverse relationship between rate of VTE prophylaxis and rate of clinical outcome of VTE would be helpful.

In conclusion, in a setting in which most hospitalized medically ill patients have multiple risk factors for VTE, we have shown that a practical multifaceted intervention can result in a marked increase in the proportion of medical patients receiving VTE prophylaxis, as well as in the proportion of patients receiving prophylaxis commensurate with evidence‐based guidelines.

Acknowledgements

We thank Nicholas Galeota, Director of Pharmacy at SUNY Downstate for his assistance in providing monthly patient medication lists, Helen Wiggett for providing writing support, and Dan Bridges for editorial support for this manuscript.

References
  1. Goldhaber SZ.Pulmonary embolism.Lancet.2004;363:12951305.
  2. Heit JA,Silverstein MD,Mohr DN,Petterson TM,O'Fallon WM,Melton LJ.Risk factors for deep vein thrombosis and pulmonary embolism: a population‐based case‐control study.Arch Intern Med.2000;160:809815.
  3. Heit JA,O'Fallon WM,Petterson TM, et al.Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population‐based study.Arch Intern Med.2002;162:12451248.
  4. Geerts WH,Pineo GF,Heit JA, et al.Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest.2004;126:338S400S.
  5. Nicolaides AN,Breddin HK,Fareed J, et al.,Cardiovascular Disease Educational and Research Trust, International Union of Angiology.Prevention of venous thromboembolism. International Consensus Statement. Guidelines compiled in accordance with the scientific evidence.Int Angiol.2001;20:137.
  6. Anderson FA,Wheeler HB,Goldberg RJ, et al.Changing clinical practice. Prospective study of the impact of continuing medical education and quality assurance programs on use of prophylaxis for venous thromboembolism.Arch Intern Med.1994;154:669677.
  7. Arnold DM,Kahn SR,Shrier I.Missed opportunities for prevention of venous thromboembolism: an evaluation of the use of thromboprophylaxis guidelines.Chest.2001;120:19641971.
  8. Aujesky D,Guignard E,Pannatier A,Cornuz J.Pharmacological thromboembolic prophylaxis in a medical ward: room for improvement.J Gen Intern Med.2002;17:788791.
  9. Learhinan ER,Alderman CP.Venous thromboembolism prophylaxis in a South Australian teaching hospital.Ann Pharmacother.2003;37:13981402.
  10. Vallano A,Arnau JM,Miralda GM,Perez‐Bartoli J.Use of venous thromboprophylaxis and adherence to guideline recommendations: a cross‐sectional study.Thromb J.2004;2:39.
  11. Cabana MD,Rand CS,Powe NR, et al.Why don't physicians follow clinical practice guidelines? A framework for improvement.JAMA.1999;282:14581465.
  12. Swan J,Spigelman AD.Audit of surgeon awareness of readmissions with venous thrombo‐embolism.Intern Med J.2003;33:578580.
  13. Zierler BK,Meissner MH,Cain K,Strandness DEA survey of physicians' knowledge and management of venous thromboembolism.Vasc Endovascular Surg.2002;36:367375.
  14. McEleny P,Bowie P,Robins JB,Brown RC.Getting a validated guideline into local practice: implementation and audit of the SIGN guideline on the prevention of deep vein thrombosis in a district general hospital.Scott Med J.1998;43:2325.
  15. Peterson GM,Drake CI,Jupe DM,Vial JH,Wilkinson S.Educational campaign to improve the prevention of postoperative venous thromboembolism.J Clin Pharm Ther.1999;24:279287.
  16. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977.
  17. Walker A,Campbell S,Grimshaw J.Implementation of a national guideline on prophylaxisof venous thromboembolism: a survey of acute services in Scotland.Thromboembolism Prevention Evaluation Study Group.Health Bull (Edinb).1999;57:141147.
  18. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  19. Tapson VF,Decousus H,Piovella F,Zotz RB,Allegrone J,Anderson FA.A multinational observational cohort study in acutely ill medical patients of practices in prevention of venous thromboembolism: findings of the international medical prevention registry on venous thromboembolism (IMPROVE).Blood.2003;102:321a.
  20. Geerts WH,Heit JA,Clagett PG, et al.Prevention of venous thromboembolism.Chest.2001;119:132S175S.
  21. Caprini JA,Arcelus JI,Reyna JJ.Effective risk stratification of surgical and nonsurgical patients for venous thromboembolic disease.Semin Hematol.2001;38(2 Suppl 5):1219.
  22. Anderson FA,Wheeler HB,Goldberg RJ,Hosmer DW,Forcier A.The prevalence of risk factors for venous thromboembolism among hospital patients.Arch Intern Med.1992;152:16601664.
  23. Stinnett JM,Pendleton R,Skordos L,Wheeler M,Rodgers GM.Venous thromboembolism prophylaxis in medically ill patients and the development of strategies to improve prophylaxis rates.Am J Hematol.2005;78:167172.
  24. Tapson VF,Goldhaber SZ.Failure to prophylax for deep vein thrombosis: results from the DVT FREE registry.Blood.2003;102:322a.
  25. Byrne GJ,McCarthy MJ,Silverman SH.Improving uptake of prophylaxis for venous thromboembolism in general surgical patients using prospective audit.BMJ.1996;313:917.
  26. Mosen D,Elliott CG,Egger MJ, et al.The effect of a computerized reminder system on the prevention of postoperative venous thromboembolism.Chest.2004;125:16351641.
  27. Beaulieu MD,Rivard M,Hudon E,Beaudoin C,Saucier D,Remondin M.Comparative trial of a short workshop designed to enhance appropriate use of screening tests by family physicians.CMAJ.2002;167:12411246.
  28. Oxman AD,Thomson MA,Davis DA,Haynes RB.No magic bullets: a systematic review of 102 trials of interventions to improve professional practice.CMAJ.1995;153:14231431.
  29. Tooher R,Middleton P,Pham C, et al.A systematic review of strategies to improve prophylaxis for venous thromboembolism in hospitals.Ann Surg.2005;241:397415.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
331-338
Legacy Keywords
prophylaxis, education, thromboembolism, guideline adherence, quality improvement
Sections
Article PDF
Article PDF

Venous thromboembolism (VTE), which encompasses both deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of the morbidity and mortality of hospitalized medical patients.1 Hospitalization for an acute medical illness has been associated with an 8‐fold increase in the relative risk of VTE and is responsible for approximately a quarter of all VTE cases in the general population.2, 3

Current evidence‐based guidelines, including those from the American College of Chest Physicians (ACCP), recommend prophylaxis with low‐dose unfractionated heparin (UFH) or low‐molecular‐weight heparin (LMWH) for medical patients with risk factors for VTE.4, 5 Mechanical prophylaxis methods including graduated compression stockings and intermittent pneumatic compression are recommended for those patients for whom anticoagulant therapy is contraindicated because of a high risk of bleeding.4, 5 However, several studies have shown that adherence to these guidelines is suboptimal, with many at‐risk patients receiving inadequate prophylaxis (range 32%‐87%).610

Physician‐related factors identified as potential barriers to guideline adherence include not being aware or familiar with the guidelines, not agreeing with the guidelines, or believing the guideline recommendations to be ineffective.11 More specific studies have shown that some physicians may lack basic knowledge regarding the current treatment standards for VTE and may underestimate the significance of VTE.1213 As distinct strategies, education aimed at disseminating VTE prophylaxis guidelines, as well as regular audit‐and‐feedback of physician performance, has been shown to improve rates of VTE prophylaxis in clinical practice.6, 1417 Implementation of educational programs significantly increased the level of appropriate VTE prophylaxis from 59% to 70% of patients in an Australian hospital15 and from 73% to 97% of patients in a Scottish hospital.14 Another strategy, the use of point‐of‐care electronically provided reminders with decision support, has been successful not only in increasing the rates of VTE prophylaxis, but also in decreasing the incidence of clinical VTE events.16 Although highly effective, electronic alerts with computerized decision support do not exist in many hospitals, and other methods of intervention are needed.

In this study, we evaluated adherence to the 2001 ACCP guidelines for VTE prophylaxis among medical patients in our teaching hospital. (The guidelines were updated in 2004, after our study was completed.) After determining that our baseline rates of appropriate VTE prophylaxis were suboptimal, we developed, implemented, and evaluated a multifaceted strategy to improve the rates of appropriate thromboprophylaxis among our medical inpatients.

Six categories of quality improvement strategies have been described: provider education, decision support, audit‐and‐feedback, patient education, organization change, and regulation and policy.18 The intervention we developed was a composite of 3 of these: provider education, decision support, and audit‐and‐feedback.

METHODS

Study Design and Patients

This was a before‐and‐after study designed to assess whether implementation of a VTE prophylaxis quality improvement intervention could improve the rate of appropriate thromboprophylaxis in hospitalized medical patients at the State University of New York, Downstate Medical CenterUniversity Hospital of Brooklyn, an urban university teaching hospital of approximately 400 beds. This initiative, conducted as part of a departmental quality assurance and performance improvement program, did not require institutional review board approval. After an informal survey revealed a prophylaxis rate of approximately 50%, a more formal baseline assessment of the rate of medical patients receiving VTE prophylaxis was conducted during October 2002. This assessment was a single sampling of all medical inpatients on 2 of the medical floors on a single day. The results were consistent with those of the informal survey as well as those from an international registry.19 The results from the baseline study indicated that VTE prophylaxis was underused: only 46.9% of our medical inpatients received any form of prophylaxis. The prophylaxis rate was assessed again in 2 sampling periods beginning 12 and 18 months after implementation of the intervention. Data were collected monthly and combined into 3‐month blocks. The first postintervention sample (n = 116 patient charts) was drawn from a period 12‐14 months after implementation and the second (n = 147 patient charts) from a period 18‐20 months after implementation.

On a randomly designated day in the latter half of each month during each sampling period, all charts on 2 primary medical floors were reviewed and included in the retrospective analysis. Patients who were not on the medical service were excluded from analysis. Patients, as well as their medications, were identified using a list generated from our pharmacy database. We chose this method and schedule for several reasons. First, we sought to reduce the likelihood of including a patient more than once in a monthly sample. Second, by waiting for the latter half of the month we sought to allow house staff a chance to acquire knowledge from the educational program introduced on the first day of the month. Third, we wanted to allow house staff the time to actualize new attitudes reinforced by the audit‐and‐feedback element. The house staff included approximately 4 interns and 4 residents each month plus 10‐15 attendings or hospitalists.

Data Collection

For each sampling period we conducted a medical record (paper) review, and the Division Chief of General Internal Medicine also interviewed the medical house staff and attending physicians. Data collected included risk factors for VTE, contraindications to anticoagulant prophylaxis, type of VTE prophylaxis received, and appropriateness of the prophylaxis. Prophylaxis was considered appropriate when it was given in accordance with a risk stratification scheme (Table 1) adapted from the 2001 ACCP guideline recommendations for surgical patients20 and modified for medical inpatients, similar to the risk assessment model by Caprini et al.21 Prophylaxis was also considered appropriate when no prophylaxis was given for low‐risk patients or when full anticoagulation was given for another indication (Table 1). Questionable prophylaxis was defined as UFH given every 12 hours to a high‐risk patient. All other prophylaxis was deemed inappropriate (including no prophylaxis if prophylaxis was indicated, use of enoxaparin at incorrect prophylactic doses such as 60 or 20 mg, IPC alone for a high‐risk patient with no contraindication to pharmacological prophylaxis, and the use of warfarin if no other indication for it). The risk factors for thromboembolism and contraindications to anticoagulant prophylaxis are given in Table 2. Non‐ambulatory was defined as an order for bed rest with or without bathroom privileges or was judged based on information obtained from the medical house staff and nurses about whether the patient was ambulatory or had been observed walking outside his or her room. Data on pharmacological prophylaxis were obtained from the hospital pharmacy. Information on use of mechanical prophylaxis was obtained by house staff interviews or review of the order sheet. The house officer or attending physician of each patient was interviewed retrospectively to determine the reason for admission and the risk factors for VTE present on admission. Patients were classified as having low, moderate, high, or highest risk for VTE based on their age and any major risk factors for VTE (Table 1).19 All collected data were reported to the Department of Medicine Performance Improvement Committee for independent corroboration.

VTE Risk Categories and Appropriate Prophylaxisa
Risk categoryDefinitionDosage of appropriate prophylaxis
Age (years)Additional risk factorsbLow‐dose unfractionated heparinLMWH
  • Appropriate prophylaxis was defined as prophylaxis in accordance with the risk stratification scheme above, which was adopted from the ACCP 2001 guideline recommendations for surgical patients19 and modified for medically ill patients; appropriate prophylaxis also included no prophylaxis for low‐risk patients or patients on full anticoagulation (with warfarin, IV UFH, or LMWH) for other indications.

  • See Table 2.

  • CVA, cerebrovascular accident; LMWH, low‐molecular‐weight heparin; q12h, every 12 hours; q8h, every 8 hours; IPC, intermittent pneumatic compression; VTE, venous thromboembolism.

Low (0‐1 risk factors)<400‐1 factorNoneNone
Moderate (2 risk factors)40‐601 factor5000 units q12h40 mg of enoxaparin or 5000 units of dalteparin
High (3‐4 risk factors)>601‐2 factors or hypercoagulable state5000 units q8h or q12h (q8h recommended for surgical patients)40 mg of enoxaparin or 5000 units of dalteparin
Highest (5 or more factors)>40Malignancy, prior VTE, or CVA5000 units q8h plus IPCenoxaparin or dalteparin plus IPC
Risk Factors for Thromboembolism and Contraindications to Anticoagulant Prophylaxis
Risk factors for thromboembolism
Contraindications to anticoagulant prophylaxis
Age > 40 years
Infection
Inflammatory disease
Congestive heart failure
Chronic obstructive pulmonary disease
Prior venous thromboembolism
Cancer
Cerebrovascular accident
End‐stage renal disease
Hypercoagulable state
Atrial fibrillation
Recent surgery
Obesity
Non‐ambulatory
Active gastrointestinal bleed
Central nervous system bleed
Thrombocytopenia (platelet count <100,000/L)

Intervention Strategies

The intervention introduced comprised 3 strategies designed to improve VTE prophylaxis: provider education, decision support, and audit‐and‐feedback.

Provider Education

On the first day of every month, an orientation was given to all incoming medicine house staff by the chief resident that included information on the scope, risk factors, and asymptomatic nature of VTE, the importance of risk stratification, the need to provide adequate prophylaxis, and recommended prophylaxis regimens. A nurse educator also provided information to the nursing staff with the expectation that they would remind physicians to prescribe prophylactic treatment if not ordered initially; however, according to the nurses and house staff, this rarely occurred. Large posters showing VTE risk factors and prophylaxis were displayed at 2 nursing stations and physician charting rooms but were not visible to patients.

Decision Support

Pocket cards containing information on VTE risk factors and prophylaxis options were handed out to the house staff at the beginning of each month. These portable decision support tools assisted physicians in the selection of prophylaxis (a more recent, revised version of the material contained in this pocket guide is available at http://www.lovenox.com/hcp/dvtProphylaxisAndTreatment/dvtMedicalProphylaxis/guidelines.aspx#chart).

Audit‐and‐Feedback

Monthly audits were performed by the Division Chief of General Internal Medicine in order to evaluate the type and appropriateness of VTE prophylaxis prescribed (Table 3). During the orientation at the beginning of the month, the chief resident mentioned that an audit would take place sometime during the rotation. This random audit took place during the last 2 weeks of each month on the same day the data were requested from the pharmacy. Over 1‐2 days, physicians were interviewed either one to one or in a group, depending on the availability of house staff. All house staff and hospitalists were queried about the reasons for admission and the presence of VTE risk factors; physicians received feedback from the Division Chief on VTE risk category, prophylaxis, and appropriateness of prophylaxis treatment of their patients.

Educational Program
ElementTime/effort required
  • VTE, venous thromboembolism.

Orientation about VTE risk factors and the need to provide adequate prophylaxis given to all incoming house staff by the chief resident on the first day of every month10 min/month
Introduction of pocket cards containing information on VTE risk factors and prophylaxis options5 min/month
In‐hospital education of nurses by the nurse educator2 sessions of 1 h
Large posters presenting VTE risk factors and prophylaxis displayed in nursing stations and physician charting rooms5 min one time only
Monthly audits by the Division Chief of General Internal Medicine to evaluate the type and suitability of VTE prophylaxis prescribed2 h/month for interviews 2 h/month for record review/ data entry

Statistical Analysis

Differences in pre‐ and post‐intervention VTE prophylaxis and appropriate VTE prophylaxis rates were analyzed using the chi‐square test for categorical variables and the one‐way analysis of variance test for continuous variables. Differences were considered significant at the 5% level (P = .05).

RESULTS

Patients and Demographics

From October 2002 to August 2004 data were collected from 312 hospitalized medical patients: 49 patients in the baseline group during October 2002, and 116 and 147 at the 12‐ to 14‐month and 18‐ to 20‐month time points, respectively. Thus, approximately 40‐50 patients were randomly selected each month, representing 40% of the general medical service census. Patient demographics were similar between groups (Table 4). Overall, most patients were female (65.7%), and mean age was 61.2 years. The most common admission diagnoses were infection/sepsis (29.5%), chest pain/acute coronary syndromes/myocardial infarction (15.7%), heart failure (10.9%), and malignancy (9.6%). Overall, 7.1% (22 patients) had a contraindication to anticoagulant prophylaxis. The most common contraindication was active gastrointestinal bleeding on the current admission, which occurred in 18 of these patients.

Patient Demographics and Proportion of Patients with Risk Factors for Thrombosis in Each Study Group
 Baseline (n = 49)12 months (n = 116)18 months (n = 147)P valuea
  • P value determined using 3‐way chi‐square test unless otherwise stated.

  • P value determined using 3‐way ANOVA.

  • Due to missing data, n = 49, 82, and 140 in the baseline, 12‐month, and 18‐month groups, respectively.

  • Significantly different from baseline, P = .02. CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

Patient demographic
Mean age, years (SE)59.3 (2.6)63.3 (1.6)60.1 (1.5).25b
Men, n (%)20 (40.8)31 (26.7)56 (38.1).08
Contraindications to pharmacological prophylaxis, n (%)7 (14.3)5 (4.3)10 (6.8).07
Gastrointestinal bleeding5 (10.2)5 (4.3)8 (5.4) 
CNS bleeding1 (2.0)0 (0.0)0 (0.0) 
Low platelet count1 (2.0)0 (0.0)2 (1.4) 
Risk factor
Mean number of risk factors (SE)3.1 (0.2)2.7 (0.1)3.0 (0.1).05b
Non‐ambulatoryc46 (93.9)73 (89.0)112 (80.0)d.03
Age > 40 years39 (79.6)101 (87.1)122 (83.0).44
Cancer14 (28.6)15 (12.9)24 (16.3).05
End‐stage renal disease13 (26.5)29 (25.0)36 (24.5).96
Congestive heart failure11 (22.4)23 (19.8)28 (19.0).87
Infection8 (16.3)24 (20.7)46 (31.3).04
Cerebrovascular accident8 (16.3)12 (10.3)15 (10.2).47
COPD5 (10.2)9 (7.8)14 (9.5).84
Sepsis3 (6.1)6 (5.2)21 (14.3).03
Atrial fibrillation3 (6.1)8 (6.9)15 (10.2).52
Surgery1 (2.0)1 (0.9)2 (1.4).82
Previous venous thromboembolism0 (0.0)6 (5.2)8 (5.4).25
Obesity (morbid)0 (0.0)2 (1.7)2 (1.4).66
Hypercoagulable state0 (0.0)0 (0.0)0 (0.0) 

Risk Factors for VTE

Patient risk factors for VTE in each data collection period are summarized in Table 4. Analysis of this data showed that the most prevalent risk factors for VTE in the 3 patient populations were age older than 40 years (262/312, 84.0% of the total patient population) and nonambulatory state (231/271, 85.2% of the total population). Overall, the average number of risk factors for VTE was approximately 3, with more than 60% of patients having 3 or more VTE risk factors (Fig. 1).

Figure 1
Distribution of number of risk factors for venous thromboembolism.

Prophylaxis Use

The types of VTE prophylaxis used and the proportion of patients treated appropriately are summarized for each data collection period in Tables 5 and 6, respectively. In all 3 populations, most patients received pharmacological rather than mechanical prophylaxis, most commonly UFH. At baseline, the prophylaxis decision was appropriate (in accordance with the recommendations of the ACCP guidelines) as often as it was inappropriate (42.9% of patients). The prophylaxis decision was questionable in the remaining 14.3% of patients.

Summary of Prophylaxis Use in Each Patient Population
Prophylaxis typeBaseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using chi‐square test compared with baseline.

  • Full‐dose intravenous anticoagulation.

  • 5000 units subcutaneously.

  • qd, Once daily; bid, twice daily; tid, 3 times daily; UFH, unfractionated heparin; LWMH, low‐molecular‐weight heparin.

Any pharmacological22 (44.9)94 (81.0)<.01118 (80.3)<.01
Any UFH17 (34.7)61 (52.6).0458 (39.5).55
IV UFHb3 (6.1)5 (4.3) 2 (1.4) 
bid UFHc13 (26.5)43 (37.1) 39 (26.5) 
tid UFHc1 (2.0)10 (8.6) 16 (10.9) 
qd UFHc0 (0.0)3 (2.6) 1 (0.7) 
Any LMWH6 (12.2)30 (25.9).0559 (40.1)<.01
Mechanical prophylaxis1 (2.0)7 (6.0).2810 (6.8).21
Warfarin6 (12.2)20 (17.2).4219 (12.9).90
Summary of Appropriate Prophylaxis Use in Each Population
 Baseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using the chi‐square test compared with baseline.

  • LWMH, low‐molecular‐weight heparin; UFH, unfractionated heparin.

Receiving prophylaxis23 (46.9)100 (86.2)<.01127 (86.4)<.01
Appropriate21 (42.9)79 (68.1)<.01125 (85.0)<.01
UFH10 (20.4)33 (28.4).2845 (30.6).16
LMWH5 (10.2)27 (23.3).0558 (39.5)<.01
Questionable7 (14.3)28 (24.1).1414 (9.5).35
Inappropriate21 (42.9)9 (7.8)<.018 (5.4)<.01

Change in Prophylaxis Use

Twelve and 18 months after implementation of the quality improvement program, we observed an increase in the use of any prophylaxis, from 46.9% at baseline to 86.2% and 86.4%, respectively (Table 5; P < .01 in both groups versus baseline). This increase was a result almost entirely of an increase in the proportion of patients receiving pharmacological prophylaxis, which significantly increased, from 44.9% to 81.0% and 80.3%, at the 12‐ and 18‐month time points, respectively (Table 5; P < .01 for both groups versus baseline). Most meaningfully, there was a significant increase in the proportion of patients for whom an appropriate prophylaxis decision was made (from 42.9% to 68.1% and 85.0%, at the 12‐ and 18‐month time points, respectively; Table 6; P < .01 for both groups versus baseline). This represented a trend toward continuing increases in the use of appropriate prophylaxis as the study progressed (Fig. 2). This change was driven mainly by a significant increase in the prescribing of LMWH, almost all of which was prescribed in accordance with the 2001 ACCP guidelines (Table 6).

Figure 2
Run chart of appropriate prophylaxis rates.

DISCUSSION

In this study we evaluated the effect of an intervention that combined physician education with a decision support tool and a mechanism for audit‐and‐feedback. We have shown that implementation of such a multifaceted intervention is practical in a teaching hospital and can improve the rates of VTE prophylaxis use in medical patients. In nearly doubling the rate of appropriate prophylaxis, the effect size of our intervention was large, statistically significant, and sustained 18 months after implementation.

More than 60% of our patients had 3 or more risk factors, and more than 80% had at least 2 risk factors. The rate we observed for patients with 3 or more risk factors was 3 times higher than that reported previously.22 Despite the prevalence of high‐risk patients in our study, we observed that the preintervention rate of VTE prophylaxis among medical patients was relatively low at 47%, and only 43% of patients received prophylaxis in accordance with the ACCP guidelines. Our study findings are consistent with those of several other studies that have shown low rates of VTE prophylaxis in medical patients.6, 8, 2324 In a study of 15 hospitals in Massachusetts, only 13%‐19% of medical patients with indications and risk factors for VTE prophylaxis received any prophylaxis prior to an educational intervention.6 Similarly, a study of 368 consecutive medical patients at a Swiss hospital showed that only 22% of those at‐risk received VTE prophylaxis in accordance with the Thromboembolic Risk Factors (THRIFT) I Consensus Group recommendations.8 Results from 2 prospective patient registries also indicated low rates of VTE prophylaxis in medical patients.19, 24 In the IMPROVE registry of acutely ill medical patients, only 39% of patients hospitalized for 3 or more days received VTE prophylaxis19 and in the DVT‐FREE registry only 42% of medical patients with the inpatient diagnosis of DVT had received prophylaxis within 30 days of that diagnosis.24 In a recent retrospective study of 217 medical patients at the University of Utah hospital, just 43% of patients at high risk for VTE received any sort of prophylaxis.23

Physician education was the main intervention in several previous studies aimed at raising rates of VTE prophylaxis. Our study joins those that have also shown significant improvements after implementation of VTE prophylaxis educational initiatives.6, 14, 15, 23 In the study by Anderson et al., a significantly greater increase in the proportion of high‐risk patients receiving effective VTE prophylaxis was seen between 1986 and 1989 in hospitals that participated in a formal continuing medical education program compared with those that did not (increase: 28% versus 11%; P < .001).6 In 3 additional studies, educational interventions were shown to increase the rate of appropriate prophylaxis in at‐risk patients from 59% to 70%, from 55% to 96%, and from 43% to 72%.14, 15, 23

Other studies have cast doubt on the ability of time‐limited educational interventions to achieve a large or sustained effect.27, 28 A recent systematic review of strategies to improve the use of prophylaxis in hospitals concluded that a number of active strategies are likely to achieve optimal outcomes by combining a system for reminding clinicians to assess patients for VTE with assisting the selection of prophylaxis and providing audit‐and‐feedback.29 The large, sustained effect reported in our study might have been a result of the multifaceted and ongoing nature of the intervention, with reintroduction of the material to all incoming house staff each month. An audit from the last quarter of 2005nearly 2 years after the start of our interventionshowed that prophylaxis rates were approaching 100% (data not included in this study).

Another strategy, the use of computerized reminders to physicians, has been shown to increase the rate of VTE prophylaxis in surgical and medical/surgical patients.16, 26 Kucher et al. compared the incidence of DVT or PE in 1255 hospitalized patients whose physicians received an electronic alert of patient risk of DVT with 1251 hospitalized patients whose physicians did not receive such an alert. They found that the computer alert was associated with a significant reduction in the incidence of DVT or PE at 90 days, with a hazard ratio of 0.59 (95% confidence interval: 0.43, 0.81).16 Our study offers one practical alternative for those institutions that, like ours, do not currently have computerized order entry.

We were unable to determine if there was a specific element of the multifaceted VTE prophylaxis intervention program that contributed the most to the improvement in prophylaxis rates. Provider education was ongoing rather than just a single educational campaign. It was further supported by the pocket cards that provided support for decision making on VTE risk factors, risk categories (based on number and type of risk factor), recommended prophylaxis choices, and potential contraindications. In addition, our method of audit‐and‐feedback constructively leveraged the Hawthorne effect: aware that individual behavior was being measured, our physicians likely adjusted their practice accordingly. Taken together, it is likely that the several elements of our intervention were more powerful in combination than they would have been alone.

Although the multifaceted intervention worked well within our urban university teaching hospital, its application and outcome might be different for other types of hospitals. In our audit‐and‐feedback, for instance, review of resident physician performance was conducted by the Division Chief of General Internal Medicine, tapping into a very strong authority gradient. Hierarchical structures are likely to be different in other types of hospitals. It would therefore be valuable to examine whether the audit‐and‐feedback methodology presented in this article can be replicated in other hospital settings.

A potential limitation of this study was the use of retrospective review to determine baseline rates of VTE prophylaxis. This approach relies on medical notes being accurate and complete; such notes may not have been available for each patient. However, random reviews of both patient charts and hospital billing data for comorbidities performed after coding as a quality control step allowed for confirmation of the data or the extraction and addition of missing data. In addition, data collection was limited to a single day in the latter half of the month. It is not clear whether this sampling strategy collects data that are reflective of performance for the entire month. Our study was also limited by the absence of a control group. Without a control group, we cannot exclude the possibility that during the study factors other than the educational intervention might have contributed to the improvement in prophylaxis rates.

In this study we did not address whether an increase in VTE prophylaxis use translates to an improvement in patient outcomes, namely, a reduction in the rate of VTE. Mosen et al. showed that increasing the VTE prophylaxis rate by implementing a computerized reminder system did not decrease the rate of VTE.26 However, the baseline rate of VTE prophylaxis was already very good, and the study was only powered to detect a large difference in VTE rates. Conversely, Kucher et al. recently demonstrated a significant reduction in VTE events 90 days after initiation of a computerized alert program.16 Further studies designed to confirm the inverse relationship between rate of VTE prophylaxis and rate of clinical outcome of VTE would be helpful.

In conclusion, in a setting in which most hospitalized medically ill patients have multiple risk factors for VTE, we have shown that a practical multifaceted intervention can result in a marked increase in the proportion of medical patients receiving VTE prophylaxis, as well as in the proportion of patients receiving prophylaxis commensurate with evidence‐based guidelines.

Acknowledgements

We thank Nicholas Galeota, Director of Pharmacy at SUNY Downstate for his assistance in providing monthly patient medication lists, Helen Wiggett for providing writing support, and Dan Bridges for editorial support for this manuscript.

Venous thromboembolism (VTE), which encompasses both deep vein thrombosis (DVT) and pulmonary embolism (PE), is a major cause of the morbidity and mortality of hospitalized medical patients.1 Hospitalization for an acute medical illness has been associated with an 8‐fold increase in the relative risk of VTE and is responsible for approximately a quarter of all VTE cases in the general population.2, 3

Current evidence‐based guidelines, including those from the American College of Chest Physicians (ACCP), recommend prophylaxis with low‐dose unfractionated heparin (UFH) or low‐molecular‐weight heparin (LMWH) for medical patients with risk factors for VTE.4, 5 Mechanical prophylaxis methods including graduated compression stockings and intermittent pneumatic compression are recommended for those patients for whom anticoagulant therapy is contraindicated because of a high risk of bleeding.4, 5 However, several studies have shown that adherence to these guidelines is suboptimal, with many at‐risk patients receiving inadequate prophylaxis (range 32%‐87%).610

Physician‐related factors identified as potential barriers to guideline adherence include not being aware or familiar with the guidelines, not agreeing with the guidelines, or believing the guideline recommendations to be ineffective.11 More specific studies have shown that some physicians may lack basic knowledge regarding the current treatment standards for VTE and may underestimate the significance of VTE.1213 As distinct strategies, education aimed at disseminating VTE prophylaxis guidelines, as well as regular audit‐and‐feedback of physician performance, has been shown to improve rates of VTE prophylaxis in clinical practice.6, 1417 Implementation of educational programs significantly increased the level of appropriate VTE prophylaxis from 59% to 70% of patients in an Australian hospital15 and from 73% to 97% of patients in a Scottish hospital.14 Another strategy, the use of point‐of‐care electronically provided reminders with decision support, has been successful not only in increasing the rates of VTE prophylaxis, but also in decreasing the incidence of clinical VTE events.16 Although highly effective, electronic alerts with computerized decision support do not exist in many hospitals, and other methods of intervention are needed.

In this study, we evaluated adherence to the 2001 ACCP guidelines for VTE prophylaxis among medical patients in our teaching hospital. (The guidelines were updated in 2004, after our study was completed.) After determining that our baseline rates of appropriate VTE prophylaxis were suboptimal, we developed, implemented, and evaluated a multifaceted strategy to improve the rates of appropriate thromboprophylaxis among our medical inpatients.

Six categories of quality improvement strategies have been described: provider education, decision support, audit‐and‐feedback, patient education, organization change, and regulation and policy.18 The intervention we developed was a composite of 3 of these: provider education, decision support, and audit‐and‐feedback.

METHODS

Study Design and Patients

This was a before‐and‐after study designed to assess whether implementation of a VTE prophylaxis quality improvement intervention could improve the rate of appropriate thromboprophylaxis in hospitalized medical patients at the State University of New York, Downstate Medical CenterUniversity Hospital of Brooklyn, an urban university teaching hospital of approximately 400 beds. This initiative, conducted as part of a departmental quality assurance and performance improvement program, did not require institutional review board approval. After an informal survey revealed a prophylaxis rate of approximately 50%, a more formal baseline assessment of the rate of medical patients receiving VTE prophylaxis was conducted during October 2002. This assessment was a single sampling of all medical inpatients on 2 of the medical floors on a single day. The results were consistent with those of the informal survey as well as those from an international registry.19 The results from the baseline study indicated that VTE prophylaxis was underused: only 46.9% of our medical inpatients received any form of prophylaxis. The prophylaxis rate was assessed again in 2 sampling periods beginning 12 and 18 months after implementation of the intervention. Data were collected monthly and combined into 3‐month blocks. The first postintervention sample (n = 116 patient charts) was drawn from a period 12‐14 months after implementation and the second (n = 147 patient charts) from a period 18‐20 months after implementation.

On a randomly designated day in the latter half of each month during each sampling period, all charts on 2 primary medical floors were reviewed and included in the retrospective analysis. Patients who were not on the medical service were excluded from analysis. Patients, as well as their medications, were identified using a list generated from our pharmacy database. We chose this method and schedule for several reasons. First, we sought to reduce the likelihood of including a patient more than once in a monthly sample. Second, by waiting for the latter half of the month we sought to allow house staff a chance to acquire knowledge from the educational program introduced on the first day of the month. Third, we wanted to allow house staff the time to actualize new attitudes reinforced by the audit‐and‐feedback element. The house staff included approximately 4 interns and 4 residents each month plus 10‐15 attendings or hospitalists.

Data Collection

For each sampling period we conducted a medical record (paper) review, and the Division Chief of General Internal Medicine also interviewed the medical house staff and attending physicians. Data collected included risk factors for VTE, contraindications to anticoagulant prophylaxis, type of VTE prophylaxis received, and appropriateness of the prophylaxis. Prophylaxis was considered appropriate when it was given in accordance with a risk stratification scheme (Table 1) adapted from the 2001 ACCP guideline recommendations for surgical patients20 and modified for medical inpatients, similar to the risk assessment model by Caprini et al.21 Prophylaxis was also considered appropriate when no prophylaxis was given for low‐risk patients or when full anticoagulation was given for another indication (Table 1). Questionable prophylaxis was defined as UFH given every 12 hours to a high‐risk patient. All other prophylaxis was deemed inappropriate (including no prophylaxis if prophylaxis was indicated, use of enoxaparin at incorrect prophylactic doses such as 60 or 20 mg, IPC alone for a high‐risk patient with no contraindication to pharmacological prophylaxis, and the use of warfarin if no other indication for it). The risk factors for thromboembolism and contraindications to anticoagulant prophylaxis are given in Table 2. Non‐ambulatory was defined as an order for bed rest with or without bathroom privileges or was judged based on information obtained from the medical house staff and nurses about whether the patient was ambulatory or had been observed walking outside his or her room. Data on pharmacological prophylaxis were obtained from the hospital pharmacy. Information on use of mechanical prophylaxis was obtained by house staff interviews or review of the order sheet. The house officer or attending physician of each patient was interviewed retrospectively to determine the reason for admission and the risk factors for VTE present on admission. Patients were classified as having low, moderate, high, or highest risk for VTE based on their age and any major risk factors for VTE (Table 1).19 All collected data were reported to the Department of Medicine Performance Improvement Committee for independent corroboration.

VTE Risk Categories and Appropriate Prophylaxisa
Risk categoryDefinitionDosage of appropriate prophylaxis
Age (years)Additional risk factorsbLow‐dose unfractionated heparinLMWH
  • Appropriate prophylaxis was defined as prophylaxis in accordance with the risk stratification scheme above, which was adopted from the ACCP 2001 guideline recommendations for surgical patients19 and modified for medically ill patients; appropriate prophylaxis also included no prophylaxis for low‐risk patients or patients on full anticoagulation (with warfarin, IV UFH, or LMWH) for other indications.

  • See Table 2.

  • CVA, cerebrovascular accident; LMWH, low‐molecular‐weight heparin; q12h, every 12 hours; q8h, every 8 hours; IPC, intermittent pneumatic compression; VTE, venous thromboembolism.

Low (0‐1 risk factors)<400‐1 factorNoneNone
Moderate (2 risk factors)40‐601 factor5000 units q12h40 mg of enoxaparin or 5000 units of dalteparin
High (3‐4 risk factors)>601‐2 factors or hypercoagulable state5000 units q8h or q12h (q8h recommended for surgical patients)40 mg of enoxaparin or 5000 units of dalteparin
Highest (5 or more factors)>40Malignancy, prior VTE, or CVA5000 units q8h plus IPCenoxaparin or dalteparin plus IPC
Risk Factors for Thromboembolism and Contraindications to Anticoagulant Prophylaxis
Risk factors for thromboembolism
Contraindications to anticoagulant prophylaxis
Age > 40 years
Infection
Inflammatory disease
Congestive heart failure
Chronic obstructive pulmonary disease
Prior venous thromboembolism
Cancer
Cerebrovascular accident
End‐stage renal disease
Hypercoagulable state
Atrial fibrillation
Recent surgery
Obesity
Non‐ambulatory
Active gastrointestinal bleed
Central nervous system bleed
Thrombocytopenia (platelet count <100,000/L)

Intervention Strategies

The intervention introduced comprised 3 strategies designed to improve VTE prophylaxis: provider education, decision support, and audit‐and‐feedback.

Provider Education

On the first day of every month, an orientation was given to all incoming medicine house staff by the chief resident that included information on the scope, risk factors, and asymptomatic nature of VTE, the importance of risk stratification, the need to provide adequate prophylaxis, and recommended prophylaxis regimens. A nurse educator also provided information to the nursing staff with the expectation that they would remind physicians to prescribe prophylactic treatment if not ordered initially; however, according to the nurses and house staff, this rarely occurred. Large posters showing VTE risk factors and prophylaxis were displayed at 2 nursing stations and physician charting rooms but were not visible to patients.

Decision Support

Pocket cards containing information on VTE risk factors and prophylaxis options were handed out to the house staff at the beginning of each month. These portable decision support tools assisted physicians in the selection of prophylaxis (a more recent, revised version of the material contained in this pocket guide is available at http://www.lovenox.com/hcp/dvtProphylaxisAndTreatment/dvtMedicalProphylaxis/guidelines.aspx#chart).

Audit‐and‐Feedback

Monthly audits were performed by the Division Chief of General Internal Medicine in order to evaluate the type and appropriateness of VTE prophylaxis prescribed (Table 3). During the orientation at the beginning of the month, the chief resident mentioned that an audit would take place sometime during the rotation. This random audit took place during the last 2 weeks of each month on the same day the data were requested from the pharmacy. Over 1‐2 days, physicians were interviewed either one to one or in a group, depending on the availability of house staff. All house staff and hospitalists were queried about the reasons for admission and the presence of VTE risk factors; physicians received feedback from the Division Chief on VTE risk category, prophylaxis, and appropriateness of prophylaxis treatment of their patients.

Educational Program
ElementTime/effort required
  • VTE, venous thromboembolism.

Orientation about VTE risk factors and the need to provide adequate prophylaxis given to all incoming house staff by the chief resident on the first day of every month10 min/month
Introduction of pocket cards containing information on VTE risk factors and prophylaxis options5 min/month
In‐hospital education of nurses by the nurse educator2 sessions of 1 h
Large posters presenting VTE risk factors and prophylaxis displayed in nursing stations and physician charting rooms5 min one time only
Monthly audits by the Division Chief of General Internal Medicine to evaluate the type and suitability of VTE prophylaxis prescribed2 h/month for interviews 2 h/month for record review/ data entry

Statistical Analysis

Differences in pre‐ and post‐intervention VTE prophylaxis and appropriate VTE prophylaxis rates were analyzed using the chi‐square test for categorical variables and the one‐way analysis of variance test for continuous variables. Differences were considered significant at the 5% level (P = .05).

RESULTS

Patients and Demographics

From October 2002 to August 2004 data were collected from 312 hospitalized medical patients: 49 patients in the baseline group during October 2002, and 116 and 147 at the 12‐ to 14‐month and 18‐ to 20‐month time points, respectively. Thus, approximately 40‐50 patients were randomly selected each month, representing 40% of the general medical service census. Patient demographics were similar between groups (Table 4). Overall, most patients were female (65.7%), and mean age was 61.2 years. The most common admission diagnoses were infection/sepsis (29.5%), chest pain/acute coronary syndromes/myocardial infarction (15.7%), heart failure (10.9%), and malignancy (9.6%). Overall, 7.1% (22 patients) had a contraindication to anticoagulant prophylaxis. The most common contraindication was active gastrointestinal bleeding on the current admission, which occurred in 18 of these patients.

Patient Demographics and Proportion of Patients with Risk Factors for Thrombosis in Each Study Group
 Baseline (n = 49)12 months (n = 116)18 months (n = 147)P valuea
  • P value determined using 3‐way chi‐square test unless otherwise stated.

  • P value determined using 3‐way ANOVA.

  • Due to missing data, n = 49, 82, and 140 in the baseline, 12‐month, and 18‐month groups, respectively.

  • Significantly different from baseline, P = .02. CNS, central nervous system; COPD, chronic obstructive pulmonary disease.

Patient demographic
Mean age, years (SE)59.3 (2.6)63.3 (1.6)60.1 (1.5).25b
Men, n (%)20 (40.8)31 (26.7)56 (38.1).08
Contraindications to pharmacological prophylaxis, n (%)7 (14.3)5 (4.3)10 (6.8).07
Gastrointestinal bleeding5 (10.2)5 (4.3)8 (5.4) 
CNS bleeding1 (2.0)0 (0.0)0 (0.0) 
Low platelet count1 (2.0)0 (0.0)2 (1.4) 
Risk factor
Mean number of risk factors (SE)3.1 (0.2)2.7 (0.1)3.0 (0.1).05b
Non‐ambulatoryc46 (93.9)73 (89.0)112 (80.0)d.03
Age > 40 years39 (79.6)101 (87.1)122 (83.0).44
Cancer14 (28.6)15 (12.9)24 (16.3).05
End‐stage renal disease13 (26.5)29 (25.0)36 (24.5).96
Congestive heart failure11 (22.4)23 (19.8)28 (19.0).87
Infection8 (16.3)24 (20.7)46 (31.3).04
Cerebrovascular accident8 (16.3)12 (10.3)15 (10.2).47
COPD5 (10.2)9 (7.8)14 (9.5).84
Sepsis3 (6.1)6 (5.2)21 (14.3).03
Atrial fibrillation3 (6.1)8 (6.9)15 (10.2).52
Surgery1 (2.0)1 (0.9)2 (1.4).82
Previous venous thromboembolism0 (0.0)6 (5.2)8 (5.4).25
Obesity (morbid)0 (0.0)2 (1.7)2 (1.4).66
Hypercoagulable state0 (0.0)0 (0.0)0 (0.0) 

Risk Factors for VTE

Patient risk factors for VTE in each data collection period are summarized in Table 4. Analysis of this data showed that the most prevalent risk factors for VTE in the 3 patient populations were age older than 40 years (262/312, 84.0% of the total patient population) and nonambulatory state (231/271, 85.2% of the total population). Overall, the average number of risk factors for VTE was approximately 3, with more than 60% of patients having 3 or more VTE risk factors (Fig. 1).

Figure 1
Distribution of number of risk factors for venous thromboembolism.

Prophylaxis Use

The types of VTE prophylaxis used and the proportion of patients treated appropriately are summarized for each data collection period in Tables 5 and 6, respectively. In all 3 populations, most patients received pharmacological rather than mechanical prophylaxis, most commonly UFH. At baseline, the prophylaxis decision was appropriate (in accordance with the recommendations of the ACCP guidelines) as often as it was inappropriate (42.9% of patients). The prophylaxis decision was questionable in the remaining 14.3% of patients.

Summary of Prophylaxis Use in Each Patient Population
Prophylaxis typeBaseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using chi‐square test compared with baseline.

  • Full‐dose intravenous anticoagulation.

  • 5000 units subcutaneously.

  • qd, Once daily; bid, twice daily; tid, 3 times daily; UFH, unfractionated heparin; LWMH, low‐molecular‐weight heparin.

Any pharmacological22 (44.9)94 (81.0)<.01118 (80.3)<.01
Any UFH17 (34.7)61 (52.6).0458 (39.5).55
IV UFHb3 (6.1)5 (4.3) 2 (1.4) 
bid UFHc13 (26.5)43 (37.1) 39 (26.5) 
tid UFHc1 (2.0)10 (8.6) 16 (10.9) 
qd UFHc0 (0.0)3 (2.6) 1 (0.7) 
Any LMWH6 (12.2)30 (25.9).0559 (40.1)<.01
Mechanical prophylaxis1 (2.0)7 (6.0).2810 (6.8).21
Warfarin6 (12.2)20 (17.2).4219 (12.9).90
Summary of Appropriate Prophylaxis Use in Each Population
 Baseline (n = 49), n (%)12 months (n = 116), n (%)P valuea18 months (n = 147), n (%)P valuea
  • P values determined using the chi‐square test compared with baseline.

  • LWMH, low‐molecular‐weight heparin; UFH, unfractionated heparin.

Receiving prophylaxis23 (46.9)100 (86.2)<.01127 (86.4)<.01
Appropriate21 (42.9)79 (68.1)<.01125 (85.0)<.01
UFH10 (20.4)33 (28.4).2845 (30.6).16
LMWH5 (10.2)27 (23.3).0558 (39.5)<.01
Questionable7 (14.3)28 (24.1).1414 (9.5).35
Inappropriate21 (42.9)9 (7.8)<.018 (5.4)<.01

Change in Prophylaxis Use

Twelve and 18 months after implementation of the quality improvement program, we observed an increase in the use of any prophylaxis, from 46.9% at baseline to 86.2% and 86.4%, respectively (Table 5; P < .01 in both groups versus baseline). This increase was a result almost entirely of an increase in the proportion of patients receiving pharmacological prophylaxis, which significantly increased, from 44.9% to 81.0% and 80.3%, at the 12‐ and 18‐month time points, respectively (Table 5; P < .01 for both groups versus baseline). Most meaningfully, there was a significant increase in the proportion of patients for whom an appropriate prophylaxis decision was made (from 42.9% to 68.1% and 85.0%, at the 12‐ and 18‐month time points, respectively; Table 6; P < .01 for both groups versus baseline). This represented a trend toward continuing increases in the use of appropriate prophylaxis as the study progressed (Fig. 2). This change was driven mainly by a significant increase in the prescribing of LMWH, almost all of which was prescribed in accordance with the 2001 ACCP guidelines (Table 6).

Figure 2
Run chart of appropriate prophylaxis rates.

DISCUSSION

In this study we evaluated the effect of an intervention that combined physician education with a decision support tool and a mechanism for audit‐and‐feedback. We have shown that implementation of such a multifaceted intervention is practical in a teaching hospital and can improve the rates of VTE prophylaxis use in medical patients. In nearly doubling the rate of appropriate prophylaxis, the effect size of our intervention was large, statistically significant, and sustained 18 months after implementation.

More than 60% of our patients had 3 or more risk factors, and more than 80% had at least 2 risk factors. The rate we observed for patients with 3 or more risk factors was 3 times higher than that reported previously.22 Despite the prevalence of high‐risk patients in our study, we observed that the preintervention rate of VTE prophylaxis among medical patients was relatively low at 47%, and only 43% of patients received prophylaxis in accordance with the ACCP guidelines. Our study findings are consistent with those of several other studies that have shown low rates of VTE prophylaxis in medical patients.6, 8, 2324 In a study of 15 hospitals in Massachusetts, only 13%‐19% of medical patients with indications and risk factors for VTE prophylaxis received any prophylaxis prior to an educational intervention.6 Similarly, a study of 368 consecutive medical patients at a Swiss hospital showed that only 22% of those at‐risk received VTE prophylaxis in accordance with the Thromboembolic Risk Factors (THRIFT) I Consensus Group recommendations.8 Results from 2 prospective patient registries also indicated low rates of VTE prophylaxis in medical patients.19, 24 In the IMPROVE registry of acutely ill medical patients, only 39% of patients hospitalized for 3 or more days received VTE prophylaxis19 and in the DVT‐FREE registry only 42% of medical patients with the inpatient diagnosis of DVT had received prophylaxis within 30 days of that diagnosis.24 In a recent retrospective study of 217 medical patients at the University of Utah hospital, just 43% of patients at high risk for VTE received any sort of prophylaxis.23

Physician education was the main intervention in several previous studies aimed at raising rates of VTE prophylaxis. Our study joins those that have also shown significant improvements after implementation of VTE prophylaxis educational initiatives.6, 14, 15, 23 In the study by Anderson et al., a significantly greater increase in the proportion of high‐risk patients receiving effective VTE prophylaxis was seen between 1986 and 1989 in hospitals that participated in a formal continuing medical education program compared with those that did not (increase: 28% versus 11%; P < .001).6 In 3 additional studies, educational interventions were shown to increase the rate of appropriate prophylaxis in at‐risk patients from 59% to 70%, from 55% to 96%, and from 43% to 72%.14, 15, 23

Other studies have cast doubt on the ability of time‐limited educational interventions to achieve a large or sustained effect.27, 28 A recent systematic review of strategies to improve the use of prophylaxis in hospitals concluded that a number of active strategies are likely to achieve optimal outcomes by combining a system for reminding clinicians to assess patients for VTE with assisting the selection of prophylaxis and providing audit‐and‐feedback.29 The large, sustained effect reported in our study might have been a result of the multifaceted and ongoing nature of the intervention, with reintroduction of the material to all incoming house staff each month. An audit from the last quarter of 2005nearly 2 years after the start of our interventionshowed that prophylaxis rates were approaching 100% (data not included in this study).

Another strategy, the use of computerized reminders to physicians, has been shown to increase the rate of VTE prophylaxis in surgical and medical/surgical patients.16, 26 Kucher et al. compared the incidence of DVT or PE in 1255 hospitalized patients whose physicians received an electronic alert of patient risk of DVT with 1251 hospitalized patients whose physicians did not receive such an alert. They found that the computer alert was associated with a significant reduction in the incidence of DVT or PE at 90 days, with a hazard ratio of 0.59 (95% confidence interval: 0.43, 0.81).16 Our study offers one practical alternative for those institutions that, like ours, do not currently have computerized order entry.

We were unable to determine if there was a specific element of the multifaceted VTE prophylaxis intervention program that contributed the most to the improvement in prophylaxis rates. Provider education was ongoing rather than just a single educational campaign. It was further supported by the pocket cards that provided support for decision making on VTE risk factors, risk categories (based on number and type of risk factor), recommended prophylaxis choices, and potential contraindications. In addition, our method of audit‐and‐feedback constructively leveraged the Hawthorne effect: aware that individual behavior was being measured, our physicians likely adjusted their practice accordingly. Taken together, it is likely that the several elements of our intervention were more powerful in combination than they would have been alone.

Although the multifaceted intervention worked well within our urban university teaching hospital, its application and outcome might be different for other types of hospitals. In our audit‐and‐feedback, for instance, review of resident physician performance was conducted by the Division Chief of General Internal Medicine, tapping into a very strong authority gradient. Hierarchical structures are likely to be different in other types of hospitals. It would therefore be valuable to examine whether the audit‐and‐feedback methodology presented in this article can be replicated in other hospital settings.

A potential limitation of this study was the use of retrospective review to determine baseline rates of VTE prophylaxis. This approach relies on medical notes being accurate and complete; such notes may not have been available for each patient. However, random reviews of both patient charts and hospital billing data for comorbidities performed after coding as a quality control step allowed for confirmation of the data or the extraction and addition of missing data. In addition, data collection was limited to a single day in the latter half of the month. It is not clear whether this sampling strategy collects data that are reflective of performance for the entire month. Our study was also limited by the absence of a control group. Without a control group, we cannot exclude the possibility that during the study factors other than the educational intervention might have contributed to the improvement in prophylaxis rates.

In this study we did not address whether an increase in VTE prophylaxis use translates to an improvement in patient outcomes, namely, a reduction in the rate of VTE. Mosen et al. showed that increasing the VTE prophylaxis rate by implementing a computerized reminder system did not decrease the rate of VTE.26 However, the baseline rate of VTE prophylaxis was already very good, and the study was only powered to detect a large difference in VTE rates. Conversely, Kucher et al. recently demonstrated a significant reduction in VTE events 90 days after initiation of a computerized alert program.16 Further studies designed to confirm the inverse relationship between rate of VTE prophylaxis and rate of clinical outcome of VTE would be helpful.

In conclusion, in a setting in which most hospitalized medically ill patients have multiple risk factors for VTE, we have shown that a practical multifaceted intervention can result in a marked increase in the proportion of medical patients receiving VTE prophylaxis, as well as in the proportion of patients receiving prophylaxis commensurate with evidence‐based guidelines.

Acknowledgements

We thank Nicholas Galeota, Director of Pharmacy at SUNY Downstate for his assistance in providing monthly patient medication lists, Helen Wiggett for providing writing support, and Dan Bridges for editorial support for this manuscript.

References
  1. Goldhaber SZ.Pulmonary embolism.Lancet.2004;363:12951305.
  2. Heit JA,Silverstein MD,Mohr DN,Petterson TM,O'Fallon WM,Melton LJ.Risk factors for deep vein thrombosis and pulmonary embolism: a population‐based case‐control study.Arch Intern Med.2000;160:809815.
  3. Heit JA,O'Fallon WM,Petterson TM, et al.Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population‐based study.Arch Intern Med.2002;162:12451248.
  4. Geerts WH,Pineo GF,Heit JA, et al.Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest.2004;126:338S400S.
  5. Nicolaides AN,Breddin HK,Fareed J, et al.,Cardiovascular Disease Educational and Research Trust, International Union of Angiology.Prevention of venous thromboembolism. International Consensus Statement. Guidelines compiled in accordance with the scientific evidence.Int Angiol.2001;20:137.
  6. Anderson FA,Wheeler HB,Goldberg RJ, et al.Changing clinical practice. Prospective study of the impact of continuing medical education and quality assurance programs on use of prophylaxis for venous thromboembolism.Arch Intern Med.1994;154:669677.
  7. Arnold DM,Kahn SR,Shrier I.Missed opportunities for prevention of venous thromboembolism: an evaluation of the use of thromboprophylaxis guidelines.Chest.2001;120:19641971.
  8. Aujesky D,Guignard E,Pannatier A,Cornuz J.Pharmacological thromboembolic prophylaxis in a medical ward: room for improvement.J Gen Intern Med.2002;17:788791.
  9. Learhinan ER,Alderman CP.Venous thromboembolism prophylaxis in a South Australian teaching hospital.Ann Pharmacother.2003;37:13981402.
  10. Vallano A,Arnau JM,Miralda GM,Perez‐Bartoli J.Use of venous thromboprophylaxis and adherence to guideline recommendations: a cross‐sectional study.Thromb J.2004;2:39.
  11. Cabana MD,Rand CS,Powe NR, et al.Why don't physicians follow clinical practice guidelines? A framework for improvement.JAMA.1999;282:14581465.
  12. Swan J,Spigelman AD.Audit of surgeon awareness of readmissions with venous thrombo‐embolism.Intern Med J.2003;33:578580.
  13. Zierler BK,Meissner MH,Cain K,Strandness DEA survey of physicians' knowledge and management of venous thromboembolism.Vasc Endovascular Surg.2002;36:367375.
  14. McEleny P,Bowie P,Robins JB,Brown RC.Getting a validated guideline into local practice: implementation and audit of the SIGN guideline on the prevention of deep vein thrombosis in a district general hospital.Scott Med J.1998;43:2325.
  15. Peterson GM,Drake CI,Jupe DM,Vial JH,Wilkinson S.Educational campaign to improve the prevention of postoperative venous thromboembolism.J Clin Pharm Ther.1999;24:279287.
  16. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977.
  17. Walker A,Campbell S,Grimshaw J.Implementation of a national guideline on prophylaxisof venous thromboembolism: a survey of acute services in Scotland.Thromboembolism Prevention Evaluation Study Group.Health Bull (Edinb).1999;57:141147.
  18. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  19. Tapson VF,Decousus H,Piovella F,Zotz RB,Allegrone J,Anderson FA.A multinational observational cohort study in acutely ill medical patients of practices in prevention of venous thromboembolism: findings of the international medical prevention registry on venous thromboembolism (IMPROVE).Blood.2003;102:321a.
  20. Geerts WH,Heit JA,Clagett PG, et al.Prevention of venous thromboembolism.Chest.2001;119:132S175S.
  21. Caprini JA,Arcelus JI,Reyna JJ.Effective risk stratification of surgical and nonsurgical patients for venous thromboembolic disease.Semin Hematol.2001;38(2 Suppl 5):1219.
  22. Anderson FA,Wheeler HB,Goldberg RJ,Hosmer DW,Forcier A.The prevalence of risk factors for venous thromboembolism among hospital patients.Arch Intern Med.1992;152:16601664.
  23. Stinnett JM,Pendleton R,Skordos L,Wheeler M,Rodgers GM.Venous thromboembolism prophylaxis in medically ill patients and the development of strategies to improve prophylaxis rates.Am J Hematol.2005;78:167172.
  24. Tapson VF,Goldhaber SZ.Failure to prophylax for deep vein thrombosis: results from the DVT FREE registry.Blood.2003;102:322a.
  25. Byrne GJ,McCarthy MJ,Silverman SH.Improving uptake of prophylaxis for venous thromboembolism in general surgical patients using prospective audit.BMJ.1996;313:917.
  26. Mosen D,Elliott CG,Egger MJ, et al.The effect of a computerized reminder system on the prevention of postoperative venous thromboembolism.Chest.2004;125:16351641.
  27. Beaulieu MD,Rivard M,Hudon E,Beaudoin C,Saucier D,Remondin M.Comparative trial of a short workshop designed to enhance appropriate use of screening tests by family physicians.CMAJ.2002;167:12411246.
  28. Oxman AD,Thomson MA,Davis DA,Haynes RB.No magic bullets: a systematic review of 102 trials of interventions to improve professional practice.CMAJ.1995;153:14231431.
  29. Tooher R,Middleton P,Pham C, et al.A systematic review of strategies to improve prophylaxis for venous thromboembolism in hospitals.Ann Surg.2005;241:397415.
References
  1. Goldhaber SZ.Pulmonary embolism.Lancet.2004;363:12951305.
  2. Heit JA,Silverstein MD,Mohr DN,Petterson TM,O'Fallon WM,Melton LJ.Risk factors for deep vein thrombosis and pulmonary embolism: a population‐based case‐control study.Arch Intern Med.2000;160:809815.
  3. Heit JA,O'Fallon WM,Petterson TM, et al.Relative impact of risk factors for deep vein thrombosis and pulmonary embolism: a population‐based study.Arch Intern Med.2002;162:12451248.
  4. Geerts WH,Pineo GF,Heit JA, et al.Prevention of venous thromboembolism: the Seventh ACCP Conference on Antithrombotic and Thrombolytic Therapy.Chest.2004;126:338S400S.
  5. Nicolaides AN,Breddin HK,Fareed J, et al.,Cardiovascular Disease Educational and Research Trust, International Union of Angiology.Prevention of venous thromboembolism. International Consensus Statement. Guidelines compiled in accordance with the scientific evidence.Int Angiol.2001;20:137.
  6. Anderson FA,Wheeler HB,Goldberg RJ, et al.Changing clinical practice. Prospective study of the impact of continuing medical education and quality assurance programs on use of prophylaxis for venous thromboembolism.Arch Intern Med.1994;154:669677.
  7. Arnold DM,Kahn SR,Shrier I.Missed opportunities for prevention of venous thromboembolism: an evaluation of the use of thromboprophylaxis guidelines.Chest.2001;120:19641971.
  8. Aujesky D,Guignard E,Pannatier A,Cornuz J.Pharmacological thromboembolic prophylaxis in a medical ward: room for improvement.J Gen Intern Med.2002;17:788791.
  9. Learhinan ER,Alderman CP.Venous thromboembolism prophylaxis in a South Australian teaching hospital.Ann Pharmacother.2003;37:13981402.
  10. Vallano A,Arnau JM,Miralda GM,Perez‐Bartoli J.Use of venous thromboprophylaxis and adherence to guideline recommendations: a cross‐sectional study.Thromb J.2004;2:39.
  11. Cabana MD,Rand CS,Powe NR, et al.Why don't physicians follow clinical practice guidelines? A framework for improvement.JAMA.1999;282:14581465.
  12. Swan J,Spigelman AD.Audit of surgeon awareness of readmissions with venous thrombo‐embolism.Intern Med J.2003;33:578580.
  13. Zierler BK,Meissner MH,Cain K,Strandness DEA survey of physicians' knowledge and management of venous thromboembolism.Vasc Endovascular Surg.2002;36:367375.
  14. McEleny P,Bowie P,Robins JB,Brown RC.Getting a validated guideline into local practice: implementation and audit of the SIGN guideline on the prevention of deep vein thrombosis in a district general hospital.Scott Med J.1998;43:2325.
  15. Peterson GM,Drake CI,Jupe DM,Vial JH,Wilkinson S.Educational campaign to improve the prevention of postoperative venous thromboembolism.J Clin Pharm Ther.1999;24:279287.
  16. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977.
  17. Walker A,Campbell S,Grimshaw J.Implementation of a national guideline on prophylaxisof venous thromboembolism: a survey of acute services in Scotland.Thromboembolism Prevention Evaluation Study Group.Health Bull (Edinb).1999;57:141147.
  18. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  19. Tapson VF,Decousus H,Piovella F,Zotz RB,Allegrone J,Anderson FA.A multinational observational cohort study in acutely ill medical patients of practices in prevention of venous thromboembolism: findings of the international medical prevention registry on venous thromboembolism (IMPROVE).Blood.2003;102:321a.
  20. Geerts WH,Heit JA,Clagett PG, et al.Prevention of venous thromboembolism.Chest.2001;119:132S175S.
  21. Caprini JA,Arcelus JI,Reyna JJ.Effective risk stratification of surgical and nonsurgical patients for venous thromboembolic disease.Semin Hematol.2001;38(2 Suppl 5):1219.
  22. Anderson FA,Wheeler HB,Goldberg RJ,Hosmer DW,Forcier A.The prevalence of risk factors for venous thromboembolism among hospital patients.Arch Intern Med.1992;152:16601664.
  23. Stinnett JM,Pendleton R,Skordos L,Wheeler M,Rodgers GM.Venous thromboembolism prophylaxis in medically ill patients and the development of strategies to improve prophylaxis rates.Am J Hematol.2005;78:167172.
  24. Tapson VF,Goldhaber SZ.Failure to prophylax for deep vein thrombosis: results from the DVT FREE registry.Blood.2003;102:322a.
  25. Byrne GJ,McCarthy MJ,Silverman SH.Improving uptake of prophylaxis for venous thromboembolism in general surgical patients using prospective audit.BMJ.1996;313:917.
  26. Mosen D,Elliott CG,Egger MJ, et al.The effect of a computerized reminder system on the prevention of postoperative venous thromboembolism.Chest.2004;125:16351641.
  27. Beaulieu MD,Rivard M,Hudon E,Beaudoin C,Saucier D,Remondin M.Comparative trial of a short workshop designed to enhance appropriate use of screening tests by family physicians.CMAJ.2002;167:12411246.
  28. Oxman AD,Thomson MA,Davis DA,Haynes RB.No magic bullets: a systematic review of 102 trials of interventions to improve professional practice.CMAJ.1995;153:14231431.
  29. Tooher R,Middleton P,Pham C, et al.A systematic review of strategies to improve prophylaxis for venous thromboembolism in hospitals.Ann Surg.2005;241:397415.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
331-338
Page Number
331-338
Article Type
Display Headline
Improved use of thromboprophylaxis for deep vein thrombosis following an educational intervention
Display Headline
Improved use of thromboprophylaxis for deep vein thrombosis following an educational intervention
Legacy Keywords
prophylaxis, education, thromboembolism, guideline adherence, quality improvement
Legacy Keywords
prophylaxis, education, thromboembolism, guideline adherence, quality improvement
Sections
Article Source

Copyright © 2006 Society of Hospital Medicine

Disallow All Ads
Correspondence Location
Department of Medicine, SUNY Downstate Medical Center, 470 Clarkson Ave, Box 68, Brooklyn, NY 11203; Fax: (718) 270‐1561
Content Gating
No Gating (article Unlocked/Free)
Alternative CME
Article PDF Media

Moxibustion burns

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
Moxibustion burns

A 53‐year‐old Korean woman was admitted to the hospital with a diagnosis of cellulitis (thin arrow) and rule out vasculitis. Further history obtained with the assistance of a Korean translator revealed that the patient, though untrained in Chinese medicine, had attempted scarring direct moxibustion for intermittent headaches. She was treated with intravenous antibiotics for 24 hours for her cellulitis and discharged in good condition on oral antibiotics.

Moxibustion is a traditional Chinese medical technique that involves burning the herb mugwort (Artemesia vulgaris) to relieve cold or stagnant conditions by stimulating circulation. Moxibustion can be performed indirectly or directly. Indirect moxibustion involves application of the burning moxa to the end of an acupuncture needle or by holding the moxa close to the skin. In direct moxibustion, a cone‐shaped moxa is held over an acupuncture point. Direct moxibustion can be divided into scarring and nonscarring types. With nonscarring direct moxibustion, moxa is placed on top of an acupuncture point, lit, and then removed before it burns the skin. With scarring moxibustion, the burning moxa is left on the skin until it burns out, leading to burns and scarring.

This case demonstrates the importance of obtaining an accurate history when making a clinical diagnosis and, in patients who are not fluent in English, the critical role that translators serve in the management of patients. The differential diagnosis of skin ulcers encompasses many other conditions in addition to infection, including iatrogenic causes of traditional as well as alternative medical therapies. 0

Figure 1
Direct moxibustion burns.

0

Figure 2
Close up of direct moxibustion burns.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
367-367
Sections
Article PDF
Article PDF

A 53‐year‐old Korean woman was admitted to the hospital with a diagnosis of cellulitis (thin arrow) and rule out vasculitis. Further history obtained with the assistance of a Korean translator revealed that the patient, though untrained in Chinese medicine, had attempted scarring direct moxibustion for intermittent headaches. She was treated with intravenous antibiotics for 24 hours for her cellulitis and discharged in good condition on oral antibiotics.

Moxibustion is a traditional Chinese medical technique that involves burning the herb mugwort (Artemesia vulgaris) to relieve cold or stagnant conditions by stimulating circulation. Moxibustion can be performed indirectly or directly. Indirect moxibustion involves application of the burning moxa to the end of an acupuncture needle or by holding the moxa close to the skin. In direct moxibustion, a cone‐shaped moxa is held over an acupuncture point. Direct moxibustion can be divided into scarring and nonscarring types. With nonscarring direct moxibustion, moxa is placed on top of an acupuncture point, lit, and then removed before it burns the skin. With scarring moxibustion, the burning moxa is left on the skin until it burns out, leading to burns and scarring.

This case demonstrates the importance of obtaining an accurate history when making a clinical diagnosis and, in patients who are not fluent in English, the critical role that translators serve in the management of patients. The differential diagnosis of skin ulcers encompasses many other conditions in addition to infection, including iatrogenic causes of traditional as well as alternative medical therapies. 0

Figure 1
Direct moxibustion burns.

0

Figure 2
Close up of direct moxibustion burns.

A 53‐year‐old Korean woman was admitted to the hospital with a diagnosis of cellulitis (thin arrow) and rule out vasculitis. Further history obtained with the assistance of a Korean translator revealed that the patient, though untrained in Chinese medicine, had attempted scarring direct moxibustion for intermittent headaches. She was treated with intravenous antibiotics for 24 hours for her cellulitis and discharged in good condition on oral antibiotics.

Moxibustion is a traditional Chinese medical technique that involves burning the herb mugwort (Artemesia vulgaris) to relieve cold or stagnant conditions by stimulating circulation. Moxibustion can be performed indirectly or directly. Indirect moxibustion involves application of the burning moxa to the end of an acupuncture needle or by holding the moxa close to the skin. In direct moxibustion, a cone‐shaped moxa is held over an acupuncture point. Direct moxibustion can be divided into scarring and nonscarring types. With nonscarring direct moxibustion, moxa is placed on top of an acupuncture point, lit, and then removed before it burns the skin. With scarring moxibustion, the burning moxa is left on the skin until it burns out, leading to burns and scarring.

This case demonstrates the importance of obtaining an accurate history when making a clinical diagnosis and, in patients who are not fluent in English, the critical role that translators serve in the management of patients. The differential diagnosis of skin ulcers encompasses many other conditions in addition to infection, including iatrogenic causes of traditional as well as alternative medical therapies. 0

Figure 1
Direct moxibustion burns.

0

Figure 2
Close up of direct moxibustion burns.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
367-367
Page Number
367-367
Article Type
Display Headline
Moxibustion burns
Display Headline
Moxibustion burns
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
California Pacific Medical Center, 2333 Buchanan St., San Francisco, CA 94115; Fax: (415) 775‐7437
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Clinical Conundrum

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
A frayed knot

A 20‐year‐old woman presented to the emergency department after 2 days of epistaxis and vaginal bleeding.

A young woman is more likely to present with infection, toxic exposure, or rheumatologic disease than with a degenerative disease or malignancy. Her bleeding may relate to a platelet abnormality, either quantitative or qualitative. I would pursue her bleeding and menstrual history further.

The patient was healthy until 2 months previously, when she noted arthralgia of her shoulders, wrists, elbows, knees, and ankles. She was examined by a rheumatologist who detected mild arthritis in her left wrist and proximal interphalangeal joints. The rest of her joints were normal. Rheumatoid factor and ANA were positive, and the erythrocyte sedimentation rate was 122 mm/hour. She was diagnosed with possible systemic lupus erythematosus and was placed on a nonsteroidal anti‐inflammatory agent. At a follow‐up visit 1 month prior to admission, her arthralgia had markedly improved. Two weeks prior to admission, the patient began to feel fatigued. Two days prior to admission, she developed epistaxis and what she thought was her menses, though bleeding was heavier than usual and associated with the passage of red clots. On the day of admission the vaginal bleeding worsened, and emergency personnel transported the patient to the hospital.

The diagnosis of systemic lupus erythematosus (SLE) is not engraved in stone. One must be vigilant for other diseases masquerading as SLE while continuing to build a case for it. As more criteria are fulfilled, the probability of lupus increases, yet no findings, alone or in combination, are pathognomonic of this protean disease. This patient's age, sex, and serology are compatible with SLE; otherwise, her presentation is nonspecific. I would request a complete blood count, coagulation tests, and additional serological tests.

The quantity of the bleeding is described, but this does not help decipher its etiology. Excess bleeding may be a result of one or more of 3 broad etiologies: problems with platelets (quantitative or qualitative), with clotting factors (quantitative or qualitative), or with blood vessels (trauma, vasculitis, or diseases affecting collagen). Because quantitative and qualitative factor disorders generally do not present with mucosal bleeding, I am thinking more about platelet problems and about processes that damage the microvasculature. If this woman has lupus, immunologic thrombocytopenia may be the cause of mucosal bleeding.

The patient had no previous medical problems and had never been pregnant. Her only medication was sulindac twice daily for the past month. She was born in Hong Kong, graduated from high school in San Francisco, and attended junior college. She lived with her parents and brother and denied alcohol, tobacco, or recreational drug use but had recently obtained a tattoo on her lower back. There was no family history of autoimmune or bleeding disorders, and a review of systems was notable for dyspnea with minimal exertion and fatigue which worsened in the past 2 days. She had no prior episodes of abnormal bleeding or clotting.

Tattoos may be surrogates for other high‐risk behaviors and suggest an increased risk of hepatitis and sexually transmitted diseases. I want to know her sexual history and other risk factors for human immunodeficiency virus infection. The dyspnea and fatigue are likely the result of anemia, but I am also considering cardiac disease. Though SLE remains a possibility, I cannot assume the presence of a lupus anticoagulant with antiphospholipid syndrome without a history of infertility or recurrent miscarriages.

On arrival at the emergency department, the patient had a blood pressure of 78/46 mm Hg, a pulse of 120 beats/min, a temperature of 34C, 14 respirations per minute, and oxygen saturation of 99% while breathing supplemental oxygen through a nonrebreather mask. Systolic blood pressure improved to 90 mmHg after 4 L of normal saline was administered. The patient was pale but alert. There was crusted blood in her mouth and nostrils without active bleeding or petechiae. Her tongue was pierced with a ring, and sclerae were anicteric. Bleeding was noted from both nipples. There was no heart murmur or gallop, and jugular venous pressure was not elevated. Pulmonary exam revealed bibasilar crackles. Abdomen was soft, not tender, and without hepatosplenomegaly, and her umbilicus was pierced by a ring. Genitourinary exam revealed scant vaginal discharge and clotted blood in the vagina. Skin demonstrated no petechiae, ecchymoses, or stigmata of liver disease. Neurological and joint exams were normal.

It is hard to conceive of vaginal bleeding producing this profound a degree of hypotension. The patient may have additional occult sites of bleeding, or she may have a distributive cause of hypotension such as sepsis or adrenal hemorrhage with resultant adrenal insufficiency. Breast bleeding is unusual, even with profound thrombocytopenia, and I wonder about a concomitant factor deficiency. Furthermore, if thrombocytopenia was the sole reason for the bleeding, I would have expected petechiae. Diffuse vascular injury, such as from lupus or vasculitis, would be an unusual cause of profound bleeding unless there was also disseminated intravascular coagulation.

Laboratory studies revealed a white count of 2000/mm3, of which 42% were neutrophils, 40% bands, 8% lymphocytes, and 10% monocytes. Hematocrit was 17.6%, platelets 35,000/mm3. Sodium was 124 mmol/L, potassium 6 mmol/L, chloride 92 mmol/L, bicarbonate 10 mmol/L, blood urea nitrogen 122 mg/dL (43.5 mmol/L), and creatinine 3.4 mg/dL (300 mol/L). Blood glucose was 44 mg/dL (2.44 mmol/L). Total bilirubin was 3.0 mg/dL (51.3 mol/L; normal range, 0.1‐1.5), alkaline phosphatase 105 U/L (normal range, 39‐117), aspartate aminotransferase 849 U/L (normal range, 8‐31), alanine aminotransferase 261 U/L (normal range, 7‐31), international normalized unit (INR) 2.9, and partial thromboplastin time (PTT) 34.2 seconds.

The combination of profound hypotension, electrolyte abnormalities, hypoglycemia, and hypothermia makes adrenal insufficiency a consideration. I would perform a cortrosyn stimulation test and start glucocorticoid and perhaps mineralocorticoid replacement. In addition, there is renal failure and metabolic acidosis, with a calculated anion gap of 22. The anion gap may be from lactic acidosis secondary to hypotension and hypoperfusion. The abnormal transaminases and bilirubin could relate to infectious hepatitis or systemic infection. Although ischemia could explain these findings, it is rare for a 20‐year‐old to develop ischemic hepatopathy. Thrombocytopenia this moderate may augment the volume of blood loss, but spontaneous bleeding because of thrombocytopenia is unusual until the platelet count falls below 20,000/mm3. Furthermore, the elevated INR points to a mixed coagulopathy. Interpretation of the INR is complicated by the fact she has liver disease, and I am most concerned about acute disseminated intravascular coagulation (DIC) or impending fulminant hepatic failure. This is not the pattern seen with antiphospholipid antibody syndrome, in which the INR tends to be preserved and the PTT prolonged.

Urine dipstick testing demonstrated a specific gravity of 1.015, trace leukocyte esterase, 2+ protein, and 3+ blood, and microscopy revealed 2 white blood cells and 38 red blood cells per high‐power field, many bacteria, and no casts. Creatine kinase was 20,599 U/L, with a myocardial fraction of 1.4%. Lipase was normal, lactate was 7.3 mmol/L, and serum pregnancy test was negative.

Although there is proteinuria and hematuria, we do not have solid evidence of glomerulonephritis. Although the red cells could be a contaminant from her vaginal bleeding, I would examine her sediment carefully for dysmorphic red cells, recognizing that only a quarter of people with glomerulonephritis have red‐cell casts. A urine protein‐to‐creatinine ratio would be useful for estimating the degree of proteinuria. The elevated creatine kinase indicates rhabdomyolysis. In a previously healthy young woman without evidence of cardiogenic shock, it would be unusual for hypotension to result in rhabdomyolysis. Infection and metabolic derangements are possible etiologies of rhabdomyolysis. Alternatively, coagulopathy might have produced intramuscular bleeding. The constellation of thrombocytopenia, anemia, and renal failure raises my suspicion that there is a thrombotic microangiopathy, such as thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS). I would inspect a peripheral‐blood smear for schistocytes and evidence of microangiopathy.

The chest radiograph demonstrated low lung volumes, patchy areas of consolidation, and pulmonary edema. Heart size was normal, and there were no pleural effusions. On the first hospital day the patient required mechanical ventilation because of respiratory failure. She received 5 units of packed red blood cells, 2 units of fresh frozen plasma, and 1 unit of platelets. Vasopressor infusion was started, and a vascular catheter was placed for hemodialysis. Blood, respiratory, and urine cultures were sent, and methylprednisolone, piperacillin/tazobactam, and vancomycin were administered. D‐dimer was greater than 10,000 ng/mL, fibrinogen was 178 mg/dL, and lactate dehydrogenase was 1671 U/L (27 kat/L). The peripheral‐blood smear demonstrated 1+ schistocytes and no spherocytes. There were fewer white blood cells with bands and myelocytes, but no blasts.

The presence of schistocytes and the elevated lactate dehydrogenase point to a microangiopathic hemolytic process. Causes of microangiopathic hemolytic anemia include TTP, HUS, DIC, paraneoplastic conditions, and endothelial damage from malignant hypertension or scleroderma renal crisis. The INR and PTT will usually be normal in TTP and HUS. The depressed fibrinogen and elevated D‐dimer suggest that in response to severe bleeding, she is also clotting. DIC, possibly from a severe infection, would explain these findings. Alternatively, the multisystem organ failure may represent progression of SLE.

Additional serology studies detected antinuclear antibodies at 1:320 with a speckled pattern. Rheumatoid factor was not present, but antidouble‐stranded DNA and antiSmith antibodies were elevated. C3 was 30 mg/dL (normal range, 90‐180), C4 was 24 mg/dL (normal range, 16‐47), and the erythrocyte sedimentation rate was 53 mm/h.

The results of the additional lab tests support a diagnosis of lupus and thus a lupus flare, but I agree that antibiotics should be empirically administered while searching for an underlying infection that might mimic lupus. Apart from infection, severe lupus may be complicated by widespread vasculitis or catastrophic antiphospholipid antibody syndrome, which would necessitate high‐dose immunosuppressive therapy and anticoagulation, respectively.

Tests for antiphospholipid antibodies including lupus anticoagulant and for anticardiolipin antibodies were negative. The patient continued to require vasopressors, hemodialysis, and mechanical ventilation. On the fourth hospital day she developed a morbilliform rash over her trunk, face, and extremities. Skin over her right buttock became indurated and tender. On the sixth day of hospitalization the skin on her face, extremities, and palms began to desquamate (Fig. 1).

Figure 1
Photographic images from hospital day 6: (A) desquamating, degloving hand rash, (B) desquamating, degloving hand rash extending onto the dorsum of the arm. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]

Regarding the rash, it is hard to differentiate the chicken from the egg. The rash may be a reaction to medication, or it may be a clue to a multiorgan disease. I am considering severe skin reactions like Stevens‐Johnson as well as bacterial toxin‐mediated diseases such as toxic shock syndrome. The criteria for toxic shock syndrome with multisystem involvement are very similar to those for lupus. In this case, a desquamating rash occurring on the heel of a multiorgan illness definitely points to toxic shock syndrome. In staphylococcal toxic shock cases, blood cultures are frequently negative, and the origin may elude detection, but of the sources identified, most have been wounds and soft‐tissue infections.

On hospital day 4, blood cultures from admission grew oxacillin‐sensitive Staphylococcus aureus in 4 of the 4 bottles. Magnetic resonance imaging of the thigh demonstrated extensive necrosis of multiple muscles (Fig. 2). The patient underwent muscle debridement in the operating room, and Gram's stain of the debrided muscle revealed Gram‐positive cocci. Following surgery, she rapidly improved. She no longer required dialysis and was eventually discharged home after completing a prolonged course of intravenous anti‐Staphylococcal antibiotics at a rehabilitation facility. Follow‐up urine testing on 2 occasions revealed 1.6 and 1.4 g of protein in 24‐hour collections, but serum creatinine remained normal, and microscopy demonstrated no dysmorphic red cells or red‐cell casts. Performance of a kidney biopsy was deferred. Other than transient arthralgia and malar rash, her lupus has been quiescent, and her prednisone dose was tapered to 5 mg daily. Six months after discharge she returned to school.

Figure 2
T1‐weighted MRI (with fat saturation) of the thighs. There is extensive liquefactive necrosis involving multiple thigh muscles that is greater in the left thigh than the right thigh.

COMMENTARY

Using the American College of Rheumatology (ACR) definition, systemic lupus erythematosus (SLE) is diagnosed when at least 4 criteria are met with a sensitivity and specificity above 95%. These criteria were developed for study purposes to differentiate SLE from other rheumatic diseases. At disease onset a patient may not meet the ACR threshold, but delaying treatment may be harmful. Data conflict on the probability of such patients eventually being classified as having SLE, with estimates ranging from less than 10% to more than 60%.1, 2 With SLE prominent in the differential diagnosis of a critically ill patient, hospitalists must consider the 3 most common causes of death in lupus patients: lupus crisis, severe infection, and thrombosis.3

Most exacerbations of SLE occur in one system, most commonly the musculoskeletal system, and are mild. However, 10% of patients a year will require high‐dose corticosteroids or cytotoxic agents for severe flares that can occur in any system affected by lupus and in 15% of cases may involve multiple sites simultaneously.4, 5 Diagnosing lupus flares remains challenging. Although pulmonary hemorrhage and red blood cell casts may strongly implicate active lupus in the lungs or kidneys, specific clinical and laboratory markers of lupus crisis are lacking. Several global indices reliably measure current disease status but are cumbersome, cannot be relied on solely for treatment decisions and have not been well studied in hospitalized patients.68 Fever, once a dependable harbinger of active lupus,9 cannot reliably discriminate lupus flares from infection. In 2 studies, Rovin et al. found that infection accounted for fever in all but one SLE outpatient taking prednisone and that in hospitalized SLE patients, failure of fevers to resolve within 48 hours of administering 20‐40 mg of prednisone daily strongly suggested infection.10 The laboratory findings provided general support for there being an SLE flare or an infection, but, as the discussant pointed out, these cannot be relied on exclusively to discriminate between the two. Results that suggest infection in an SLE patient include leukocytosis, increased band forms or metamyelocytes, and possibly elevated C‐reactive protein. Findings favoring SLE flare include leukopenia, low C3 or C4 (particularly for nephritis or hematologic flares) and elevated anti‐double‐stranded DNA antibodies for nephritis.1113 Without a clear gold standard for definitively determining a lupus crisis, it is diagnosed when clinical manifestations fit a pattern seen in SLE (nephritis, cerebritis, serositis, vasculitis, pneumonitis), the results of serology studies support this conclusion, and other plausible diagnoses are excluded.

Infection and active disease account for most ICU admissions of lupus patients. SLE and infection intertwine in 3 ways. First, SLE patients are predisposed to infection, possibly because of a variety of identified genetic abnormalities of immune function.14 Although community‐acquired bacteria and viruses account for most infections, lupus patients are vulnerable to a wide array of atypical and opportunistic pathogens. Clinical factors that augment this intrinsic risk include severity of the underlying SLE, flares of the central nervous system or kidneys, and use of immunosuppressive agents.14 The latter deserves particular attention, as a recent study found more than 90% of SLE patients admitted to an ICU with severe infection were taking corticosteroids prior to hospitalization.15 Second, infection may trigger a lupus flare. Third, features of severe lupus flares and infection may overlap. Differentiating between the 2 may be difficult, and the stakes are high, as SLE patients admitted to ICUs have a risk of death that is substantially higher (47%) than that of those without SLE (29%) and much greater than the overall risk of death for those with SLE, for whom 10‐year survival exceeds 90%.15

In addition to lupus crisis and infection, the differential diagnosis of acute multisystem disease in a patient with SLE includes catastrophic antiphospholipid syndrome (APS) and thrombotic thrombocytopenic purpura, 2 thrombotic microangiopathies to which SLE patients are predisposed. Thrombocytopenia and hemolytic anemia with schistocytes should raise suspicion of these diagnoses. Additional findings for TTP include fevers, altered mental status, acute renal failure, and elevated serum lactate dehydrogenase; however, prothrombin time should not be prolonged. Lupus anticoagulant or anticardiolipin antibodies are found in up to 30% of lupus patients, of whom 50%‐70% develop APS within 20 years, characterized by thrombosis or spontaneous abortions in the presence of antiphospholipid antibodies.16 Catastrophic APS is a rare subset of APS involving thromboses of multiple organs simultaneously and has a mortality rate of 50%.

In the present patient, an elevated INR, bleeding, hypotension, and the absence of antiphospholipid antibodies argued against TTP and APS, leading the discussant to focus on SLE and sepsis. Arthralgia, cytopenia, and the results of serology studies suggested a lupus crisis, but hypothermia, hypotension, and DIC pointed to severe infection. Empiric treatment of both conditions with corticosteroids and broad‐spectrum antibiotics was indicated, and ultimately the patient's condition was found to meet criteria for toxic shock syndrome (TSS) and SLE. TSS has rarely been reported in SLE1718 and poses a particularly difficult diagnostic challenge because a severe lupus flare can meet the diagnostic criteria for TSS (Table 1), especially early on, before the characteristic desquamating rash appears. Acuity of the illness increased the ante in this challenging case. Afraid not to treat a potentially life‐threatening condition, empiric treatment of severe lupus and sepsis was initiated. Attention then shifted to fraying, or unraveling, the knot linking infection and lupus. Ultimately, diagnoses of both TSS and SLE were established.

Criteria for Toxic Shock Syndrome
  • As listed in the Morbidity and Mortality Weekly Report.19

1. Fever > 38.9C
2. Hypotension (SBP 90 mm Hg)
3. Diffuse erythroderma
4. Desquamation, particularly of palms and soles (occurring 1‐2 weeks after onset of illness)
5. Involvement of 3 or more systems:
GI (vomiting or diarrhea at onset)
Muscular (CK > twice the upper limit of normal or severe myalgia)
Mucus membranes (vaginal, oropharyngeal, or conjunctival hyperemia)
Renal (pyuria; BUN or creatinine > twice the upper limit of normal)
Hepatic (bilirubin or transaminases > twice the upper limit of normal)
Hematologic (platelets < 100,000/mm3)
Central nervous system (altered mental status without localizing deficits unexplained by hypotension or fever)
In addition, negative cultures of blood, throat, and cerebrospinal fluid are expected (except for blood cultures in S. aureus TSS, which may be positive).

Acknowledgements

The authors thank Michael Chan, MD, and Shelley Gordon, MD, for their input on this manuscript.

References
  1. Greer JM,Panush RS.Incomplete lupus erythematosus.Arch Intern Med.1989;149:24732476.
  2. Lom‐Orta H,Alarcon‐Segovia D,Diaz‐Jouanen E.Systemic lupus erythematosus. Differences between patients who do, and who do not, fulfill classification criteria at the time of diagnosis.J Rheumatol.1980;7:831837.
  3. Cervera R,Khamashta MA,Font J, et al.Morbidity and mortality in systemic lupus erythematosus during a 10‐year period: a comparison of early and late manifestations in a cohort of 1,000 patients.Medicine (Baltimore).2003;82:299308.
  4. Gordon C,Sutcliffe N,Skan J,Stoll T,Isenberg DA.Definition and treatment of lupus flares measured by the BILAG index.Rheumatology.2003;42:13721379.
  5. Ehrenstein MR,Conroy SE,Heath J,Latchman DS,Isenberg DA.The occurrence, nature and distributions of flares in a cohort of patients with systemic lupus erythematosus: a rheumatologic view.Br J Rheumatol.1995;34:257260.
  6. Ward MM,Marx AS,Barry NN.Comparison of the validity and sensitivity to change of 5 activity indices in systemic lupus erythematosus.J Rheumatol.2000;27:664670.
  7. Walz LeBlanc BA,Gladman DD,Urowitz, MB.Serologically active clinically quiescent systemic lupus erythematosus—predictors of clinical flares.J Rheumatol.1994;21:22392241.
  8. Esdaile JM,Abrahamowicz M,Joseph L,MacKenzie T,Li Y,Danoff D.Laboratory tests as predictors of disease exacerbations in systemic lupus erythematosus. Why some tests fail.Arthritis Rheum.1996;39:370378.
  9. Stahl NI,Klippel JH,Decker JL.Fever in systemic lupus erythematosus.Am J Med.1979;67:935940.
  10. Rovin BH,Tang Y,Sun J, et al.Clinical significance of fever in the systemic lupus erythematosus patient receiving steroid therapy.Kidney Int.2005;68:747759.
  11. Sidiropoulos PI,Kritikos HD,Boumpas DT.Lupus nephritis flares.Lupus.2005;14:4952.
  12. Ho A,Barr SG,Magder LS,Petri M.A decrease in complement is associated with increased renal and hematologic activity in patients with systemic lupus erythematosus.Arthritis Rheum.2001;44:23502357.
  13. Petri M,Genovese M,Engle E,Hochberg M.Definition, incidence, and clinical description of flare in systemic lupus erythematosus. A prospective cohort study.Arthritis Rheum.1991;34:937944.
  14. Zandman‐Goddard G,Shoenfeld Y.Infections and SLE.Autoimmunity.2005;38:473485.
  15. Hsu CL,Chen KY,Yeh PS, et al.Outcome and prognostic factors in critically ill patients with systemic lupus erythematosus: a retrospective study.Critical Care.2005;9:R177R183.
  16. Levine JS,Branch DW,Rauch J.The Antiphospholipid Syndrome.N Engl J Med.2002;346:752763.
  17. Chan RMT,Graham HR,Birmingham CL.Toxic shock syndrome in a patient with systemic lupus erythematosus.Can Med Assoc J.1983;129:12011202.
  18. Huseyin TS,Maynard JP,Leach RD.Toxic shock syndrome in a patient with breast cancer and systemic lupus erythematosus.Eur J Surg Oncol.2001;27:330331.
  19. Case definitions for infectious conditions under public health surveillance.MMWR Recomm Rep.1997;46(RR‐10):39.
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
361-366
Sections
Article PDF
Article PDF

A 20‐year‐old woman presented to the emergency department after 2 days of epistaxis and vaginal bleeding.

A young woman is more likely to present with infection, toxic exposure, or rheumatologic disease than with a degenerative disease or malignancy. Her bleeding may relate to a platelet abnormality, either quantitative or qualitative. I would pursue her bleeding and menstrual history further.

The patient was healthy until 2 months previously, when she noted arthralgia of her shoulders, wrists, elbows, knees, and ankles. She was examined by a rheumatologist who detected mild arthritis in her left wrist and proximal interphalangeal joints. The rest of her joints were normal. Rheumatoid factor and ANA were positive, and the erythrocyte sedimentation rate was 122 mm/hour. She was diagnosed with possible systemic lupus erythematosus and was placed on a nonsteroidal anti‐inflammatory agent. At a follow‐up visit 1 month prior to admission, her arthralgia had markedly improved. Two weeks prior to admission, the patient began to feel fatigued. Two days prior to admission, she developed epistaxis and what she thought was her menses, though bleeding was heavier than usual and associated with the passage of red clots. On the day of admission the vaginal bleeding worsened, and emergency personnel transported the patient to the hospital.

The diagnosis of systemic lupus erythematosus (SLE) is not engraved in stone. One must be vigilant for other diseases masquerading as SLE while continuing to build a case for it. As more criteria are fulfilled, the probability of lupus increases, yet no findings, alone or in combination, are pathognomonic of this protean disease. This patient's age, sex, and serology are compatible with SLE; otherwise, her presentation is nonspecific. I would request a complete blood count, coagulation tests, and additional serological tests.

The quantity of the bleeding is described, but this does not help decipher its etiology. Excess bleeding may be a result of one or more of 3 broad etiologies: problems with platelets (quantitative or qualitative), with clotting factors (quantitative or qualitative), or with blood vessels (trauma, vasculitis, or diseases affecting collagen). Because quantitative and qualitative factor disorders generally do not present with mucosal bleeding, I am thinking more about platelet problems and about processes that damage the microvasculature. If this woman has lupus, immunologic thrombocytopenia may be the cause of mucosal bleeding.

The patient had no previous medical problems and had never been pregnant. Her only medication was sulindac twice daily for the past month. She was born in Hong Kong, graduated from high school in San Francisco, and attended junior college. She lived with her parents and brother and denied alcohol, tobacco, or recreational drug use but had recently obtained a tattoo on her lower back. There was no family history of autoimmune or bleeding disorders, and a review of systems was notable for dyspnea with minimal exertion and fatigue which worsened in the past 2 days. She had no prior episodes of abnormal bleeding or clotting.

Tattoos may be surrogates for other high‐risk behaviors and suggest an increased risk of hepatitis and sexually transmitted diseases. I want to know her sexual history and other risk factors for human immunodeficiency virus infection. The dyspnea and fatigue are likely the result of anemia, but I am also considering cardiac disease. Though SLE remains a possibility, I cannot assume the presence of a lupus anticoagulant with antiphospholipid syndrome without a history of infertility or recurrent miscarriages.

On arrival at the emergency department, the patient had a blood pressure of 78/46 mm Hg, a pulse of 120 beats/min, a temperature of 34C, 14 respirations per minute, and oxygen saturation of 99% while breathing supplemental oxygen through a nonrebreather mask. Systolic blood pressure improved to 90 mmHg after 4 L of normal saline was administered. The patient was pale but alert. There was crusted blood in her mouth and nostrils without active bleeding or petechiae. Her tongue was pierced with a ring, and sclerae were anicteric. Bleeding was noted from both nipples. There was no heart murmur or gallop, and jugular venous pressure was not elevated. Pulmonary exam revealed bibasilar crackles. Abdomen was soft, not tender, and without hepatosplenomegaly, and her umbilicus was pierced by a ring. Genitourinary exam revealed scant vaginal discharge and clotted blood in the vagina. Skin demonstrated no petechiae, ecchymoses, or stigmata of liver disease. Neurological and joint exams were normal.

It is hard to conceive of vaginal bleeding producing this profound a degree of hypotension. The patient may have additional occult sites of bleeding, or she may have a distributive cause of hypotension such as sepsis or adrenal hemorrhage with resultant adrenal insufficiency. Breast bleeding is unusual, even with profound thrombocytopenia, and I wonder about a concomitant factor deficiency. Furthermore, if thrombocytopenia was the sole reason for the bleeding, I would have expected petechiae. Diffuse vascular injury, such as from lupus or vasculitis, would be an unusual cause of profound bleeding unless there was also disseminated intravascular coagulation.

Laboratory studies revealed a white count of 2000/mm3, of which 42% were neutrophils, 40% bands, 8% lymphocytes, and 10% monocytes. Hematocrit was 17.6%, platelets 35,000/mm3. Sodium was 124 mmol/L, potassium 6 mmol/L, chloride 92 mmol/L, bicarbonate 10 mmol/L, blood urea nitrogen 122 mg/dL (43.5 mmol/L), and creatinine 3.4 mg/dL (300 mol/L). Blood glucose was 44 mg/dL (2.44 mmol/L). Total bilirubin was 3.0 mg/dL (51.3 mol/L; normal range, 0.1‐1.5), alkaline phosphatase 105 U/L (normal range, 39‐117), aspartate aminotransferase 849 U/L (normal range, 8‐31), alanine aminotransferase 261 U/L (normal range, 7‐31), international normalized unit (INR) 2.9, and partial thromboplastin time (PTT) 34.2 seconds.

The combination of profound hypotension, electrolyte abnormalities, hypoglycemia, and hypothermia makes adrenal insufficiency a consideration. I would perform a cortrosyn stimulation test and start glucocorticoid and perhaps mineralocorticoid replacement. In addition, there is renal failure and metabolic acidosis, with a calculated anion gap of 22. The anion gap may be from lactic acidosis secondary to hypotension and hypoperfusion. The abnormal transaminases and bilirubin could relate to infectious hepatitis or systemic infection. Although ischemia could explain these findings, it is rare for a 20‐year‐old to develop ischemic hepatopathy. Thrombocytopenia this moderate may augment the volume of blood loss, but spontaneous bleeding because of thrombocytopenia is unusual until the platelet count falls below 20,000/mm3. Furthermore, the elevated INR points to a mixed coagulopathy. Interpretation of the INR is complicated by the fact she has liver disease, and I am most concerned about acute disseminated intravascular coagulation (DIC) or impending fulminant hepatic failure. This is not the pattern seen with antiphospholipid antibody syndrome, in which the INR tends to be preserved and the PTT prolonged.

Urine dipstick testing demonstrated a specific gravity of 1.015, trace leukocyte esterase, 2+ protein, and 3+ blood, and microscopy revealed 2 white blood cells and 38 red blood cells per high‐power field, many bacteria, and no casts. Creatine kinase was 20,599 U/L, with a myocardial fraction of 1.4%. Lipase was normal, lactate was 7.3 mmol/L, and serum pregnancy test was negative.

Although there is proteinuria and hematuria, we do not have solid evidence of glomerulonephritis. Although the red cells could be a contaminant from her vaginal bleeding, I would examine her sediment carefully for dysmorphic red cells, recognizing that only a quarter of people with glomerulonephritis have red‐cell casts. A urine protein‐to‐creatinine ratio would be useful for estimating the degree of proteinuria. The elevated creatine kinase indicates rhabdomyolysis. In a previously healthy young woman without evidence of cardiogenic shock, it would be unusual for hypotension to result in rhabdomyolysis. Infection and metabolic derangements are possible etiologies of rhabdomyolysis. Alternatively, coagulopathy might have produced intramuscular bleeding. The constellation of thrombocytopenia, anemia, and renal failure raises my suspicion that there is a thrombotic microangiopathy, such as thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS). I would inspect a peripheral‐blood smear for schistocytes and evidence of microangiopathy.

The chest radiograph demonstrated low lung volumes, patchy areas of consolidation, and pulmonary edema. Heart size was normal, and there were no pleural effusions. On the first hospital day the patient required mechanical ventilation because of respiratory failure. She received 5 units of packed red blood cells, 2 units of fresh frozen plasma, and 1 unit of platelets. Vasopressor infusion was started, and a vascular catheter was placed for hemodialysis. Blood, respiratory, and urine cultures were sent, and methylprednisolone, piperacillin/tazobactam, and vancomycin were administered. D‐dimer was greater than 10,000 ng/mL, fibrinogen was 178 mg/dL, and lactate dehydrogenase was 1671 U/L (27 kat/L). The peripheral‐blood smear demonstrated 1+ schistocytes and no spherocytes. There were fewer white blood cells with bands and myelocytes, but no blasts.

The presence of schistocytes and the elevated lactate dehydrogenase point to a microangiopathic hemolytic process. Causes of microangiopathic hemolytic anemia include TTP, HUS, DIC, paraneoplastic conditions, and endothelial damage from malignant hypertension or scleroderma renal crisis. The INR and PTT will usually be normal in TTP and HUS. The depressed fibrinogen and elevated D‐dimer suggest that in response to severe bleeding, she is also clotting. DIC, possibly from a severe infection, would explain these findings. Alternatively, the multisystem organ failure may represent progression of SLE.

Additional serology studies detected antinuclear antibodies at 1:320 with a speckled pattern. Rheumatoid factor was not present, but antidouble‐stranded DNA and antiSmith antibodies were elevated. C3 was 30 mg/dL (normal range, 90‐180), C4 was 24 mg/dL (normal range, 16‐47), and the erythrocyte sedimentation rate was 53 mm/h.

The results of the additional lab tests support a diagnosis of lupus and thus a lupus flare, but I agree that antibiotics should be empirically administered while searching for an underlying infection that might mimic lupus. Apart from infection, severe lupus may be complicated by widespread vasculitis or catastrophic antiphospholipid antibody syndrome, which would necessitate high‐dose immunosuppressive therapy and anticoagulation, respectively.

Tests for antiphospholipid antibodies including lupus anticoagulant and for anticardiolipin antibodies were negative. The patient continued to require vasopressors, hemodialysis, and mechanical ventilation. On the fourth hospital day she developed a morbilliform rash over her trunk, face, and extremities. Skin over her right buttock became indurated and tender. On the sixth day of hospitalization the skin on her face, extremities, and palms began to desquamate (Fig. 1).

Figure 1
Photographic images from hospital day 6: (A) desquamating, degloving hand rash, (B) desquamating, degloving hand rash extending onto the dorsum of the arm. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]

Regarding the rash, it is hard to differentiate the chicken from the egg. The rash may be a reaction to medication, or it may be a clue to a multiorgan disease. I am considering severe skin reactions like Stevens‐Johnson as well as bacterial toxin‐mediated diseases such as toxic shock syndrome. The criteria for toxic shock syndrome with multisystem involvement are very similar to those for lupus. In this case, a desquamating rash occurring on the heel of a multiorgan illness definitely points to toxic shock syndrome. In staphylococcal toxic shock cases, blood cultures are frequently negative, and the origin may elude detection, but of the sources identified, most have been wounds and soft‐tissue infections.

On hospital day 4, blood cultures from admission grew oxacillin‐sensitive Staphylococcus aureus in 4 of the 4 bottles. Magnetic resonance imaging of the thigh demonstrated extensive necrosis of multiple muscles (Fig. 2). The patient underwent muscle debridement in the operating room, and Gram's stain of the debrided muscle revealed Gram‐positive cocci. Following surgery, she rapidly improved. She no longer required dialysis and was eventually discharged home after completing a prolonged course of intravenous anti‐Staphylococcal antibiotics at a rehabilitation facility. Follow‐up urine testing on 2 occasions revealed 1.6 and 1.4 g of protein in 24‐hour collections, but serum creatinine remained normal, and microscopy demonstrated no dysmorphic red cells or red‐cell casts. Performance of a kidney biopsy was deferred. Other than transient arthralgia and malar rash, her lupus has been quiescent, and her prednisone dose was tapered to 5 mg daily. Six months after discharge she returned to school.

Figure 2
T1‐weighted MRI (with fat saturation) of the thighs. There is extensive liquefactive necrosis involving multiple thigh muscles that is greater in the left thigh than the right thigh.

COMMENTARY

Using the American College of Rheumatology (ACR) definition, systemic lupus erythematosus (SLE) is diagnosed when at least 4 criteria are met with a sensitivity and specificity above 95%. These criteria were developed for study purposes to differentiate SLE from other rheumatic diseases. At disease onset a patient may not meet the ACR threshold, but delaying treatment may be harmful. Data conflict on the probability of such patients eventually being classified as having SLE, with estimates ranging from less than 10% to more than 60%.1, 2 With SLE prominent in the differential diagnosis of a critically ill patient, hospitalists must consider the 3 most common causes of death in lupus patients: lupus crisis, severe infection, and thrombosis.3

Most exacerbations of SLE occur in one system, most commonly the musculoskeletal system, and are mild. However, 10% of patients a year will require high‐dose corticosteroids or cytotoxic agents for severe flares that can occur in any system affected by lupus and in 15% of cases may involve multiple sites simultaneously.4, 5 Diagnosing lupus flares remains challenging. Although pulmonary hemorrhage and red blood cell casts may strongly implicate active lupus in the lungs or kidneys, specific clinical and laboratory markers of lupus crisis are lacking. Several global indices reliably measure current disease status but are cumbersome, cannot be relied on solely for treatment decisions and have not been well studied in hospitalized patients.68 Fever, once a dependable harbinger of active lupus,9 cannot reliably discriminate lupus flares from infection. In 2 studies, Rovin et al. found that infection accounted for fever in all but one SLE outpatient taking prednisone and that in hospitalized SLE patients, failure of fevers to resolve within 48 hours of administering 20‐40 mg of prednisone daily strongly suggested infection.10 The laboratory findings provided general support for there being an SLE flare or an infection, but, as the discussant pointed out, these cannot be relied on exclusively to discriminate between the two. Results that suggest infection in an SLE patient include leukocytosis, increased band forms or metamyelocytes, and possibly elevated C‐reactive protein. Findings favoring SLE flare include leukopenia, low C3 or C4 (particularly for nephritis or hematologic flares) and elevated anti‐double‐stranded DNA antibodies for nephritis.1113 Without a clear gold standard for definitively determining a lupus crisis, it is diagnosed when clinical manifestations fit a pattern seen in SLE (nephritis, cerebritis, serositis, vasculitis, pneumonitis), the results of serology studies support this conclusion, and other plausible diagnoses are excluded.

Infection and active disease account for most ICU admissions of lupus patients. SLE and infection intertwine in 3 ways. First, SLE patients are predisposed to infection, possibly because of a variety of identified genetic abnormalities of immune function.14 Although community‐acquired bacteria and viruses account for most infections, lupus patients are vulnerable to a wide array of atypical and opportunistic pathogens. Clinical factors that augment this intrinsic risk include severity of the underlying SLE, flares of the central nervous system or kidneys, and use of immunosuppressive agents.14 The latter deserves particular attention, as a recent study found more than 90% of SLE patients admitted to an ICU with severe infection were taking corticosteroids prior to hospitalization.15 Second, infection may trigger a lupus flare. Third, features of severe lupus flares and infection may overlap. Differentiating between the 2 may be difficult, and the stakes are high, as SLE patients admitted to ICUs have a risk of death that is substantially higher (47%) than that of those without SLE (29%) and much greater than the overall risk of death for those with SLE, for whom 10‐year survival exceeds 90%.15

In addition to lupus crisis and infection, the differential diagnosis of acute multisystem disease in a patient with SLE includes catastrophic antiphospholipid syndrome (APS) and thrombotic thrombocytopenic purpura, 2 thrombotic microangiopathies to which SLE patients are predisposed. Thrombocytopenia and hemolytic anemia with schistocytes should raise suspicion of these diagnoses. Additional findings for TTP include fevers, altered mental status, acute renal failure, and elevated serum lactate dehydrogenase; however, prothrombin time should not be prolonged. Lupus anticoagulant or anticardiolipin antibodies are found in up to 30% of lupus patients, of whom 50%‐70% develop APS within 20 years, characterized by thrombosis or spontaneous abortions in the presence of antiphospholipid antibodies.16 Catastrophic APS is a rare subset of APS involving thromboses of multiple organs simultaneously and has a mortality rate of 50%.

In the present patient, an elevated INR, bleeding, hypotension, and the absence of antiphospholipid antibodies argued against TTP and APS, leading the discussant to focus on SLE and sepsis. Arthralgia, cytopenia, and the results of serology studies suggested a lupus crisis, but hypothermia, hypotension, and DIC pointed to severe infection. Empiric treatment of both conditions with corticosteroids and broad‐spectrum antibiotics was indicated, and ultimately the patient's condition was found to meet criteria for toxic shock syndrome (TSS) and SLE. TSS has rarely been reported in SLE1718 and poses a particularly difficult diagnostic challenge because a severe lupus flare can meet the diagnostic criteria for TSS (Table 1), especially early on, before the characteristic desquamating rash appears. Acuity of the illness increased the ante in this challenging case. Afraid not to treat a potentially life‐threatening condition, empiric treatment of severe lupus and sepsis was initiated. Attention then shifted to fraying, or unraveling, the knot linking infection and lupus. Ultimately, diagnoses of both TSS and SLE were established.

Criteria for Toxic Shock Syndrome
  • As listed in the Morbidity and Mortality Weekly Report.19

1. Fever > 38.9C
2. Hypotension (SBP 90 mm Hg)
3. Diffuse erythroderma
4. Desquamation, particularly of palms and soles (occurring 1‐2 weeks after onset of illness)
5. Involvement of 3 or more systems:
GI (vomiting or diarrhea at onset)
Muscular (CK > twice the upper limit of normal or severe myalgia)
Mucus membranes (vaginal, oropharyngeal, or conjunctival hyperemia)
Renal (pyuria; BUN or creatinine > twice the upper limit of normal)
Hepatic (bilirubin or transaminases > twice the upper limit of normal)
Hematologic (platelets < 100,000/mm3)
Central nervous system (altered mental status without localizing deficits unexplained by hypotension or fever)
In addition, negative cultures of blood, throat, and cerebrospinal fluid are expected (except for blood cultures in S. aureus TSS, which may be positive).

Acknowledgements

The authors thank Michael Chan, MD, and Shelley Gordon, MD, for their input on this manuscript.

A 20‐year‐old woman presented to the emergency department after 2 days of epistaxis and vaginal bleeding.

A young woman is more likely to present with infection, toxic exposure, or rheumatologic disease than with a degenerative disease or malignancy. Her bleeding may relate to a platelet abnormality, either quantitative or qualitative. I would pursue her bleeding and menstrual history further.

The patient was healthy until 2 months previously, when she noted arthralgia of her shoulders, wrists, elbows, knees, and ankles. She was examined by a rheumatologist who detected mild arthritis in her left wrist and proximal interphalangeal joints. The rest of her joints were normal. Rheumatoid factor and ANA were positive, and the erythrocyte sedimentation rate was 122 mm/hour. She was diagnosed with possible systemic lupus erythematosus and was placed on a nonsteroidal anti‐inflammatory agent. At a follow‐up visit 1 month prior to admission, her arthralgia had markedly improved. Two weeks prior to admission, the patient began to feel fatigued. Two days prior to admission, she developed epistaxis and what she thought was her menses, though bleeding was heavier than usual and associated with the passage of red clots. On the day of admission the vaginal bleeding worsened, and emergency personnel transported the patient to the hospital.

The diagnosis of systemic lupus erythematosus (SLE) is not engraved in stone. One must be vigilant for other diseases masquerading as SLE while continuing to build a case for it. As more criteria are fulfilled, the probability of lupus increases, yet no findings, alone or in combination, are pathognomonic of this protean disease. This patient's age, sex, and serology are compatible with SLE; otherwise, her presentation is nonspecific. I would request a complete blood count, coagulation tests, and additional serological tests.

The quantity of the bleeding is described, but this does not help decipher its etiology. Excess bleeding may be a result of one or more of 3 broad etiologies: problems with platelets (quantitative or qualitative), with clotting factors (quantitative or qualitative), or with blood vessels (trauma, vasculitis, or diseases affecting collagen). Because quantitative and qualitative factor disorders generally do not present with mucosal bleeding, I am thinking more about platelet problems and about processes that damage the microvasculature. If this woman has lupus, immunologic thrombocytopenia may be the cause of mucosal bleeding.

The patient had no previous medical problems and had never been pregnant. Her only medication was sulindac twice daily for the past month. She was born in Hong Kong, graduated from high school in San Francisco, and attended junior college. She lived with her parents and brother and denied alcohol, tobacco, or recreational drug use but had recently obtained a tattoo on her lower back. There was no family history of autoimmune or bleeding disorders, and a review of systems was notable for dyspnea with minimal exertion and fatigue which worsened in the past 2 days. She had no prior episodes of abnormal bleeding or clotting.

Tattoos may be surrogates for other high‐risk behaviors and suggest an increased risk of hepatitis and sexually transmitted diseases. I want to know her sexual history and other risk factors for human immunodeficiency virus infection. The dyspnea and fatigue are likely the result of anemia, but I am also considering cardiac disease. Though SLE remains a possibility, I cannot assume the presence of a lupus anticoagulant with antiphospholipid syndrome without a history of infertility or recurrent miscarriages.

On arrival at the emergency department, the patient had a blood pressure of 78/46 mm Hg, a pulse of 120 beats/min, a temperature of 34C, 14 respirations per minute, and oxygen saturation of 99% while breathing supplemental oxygen through a nonrebreather mask. Systolic blood pressure improved to 90 mmHg after 4 L of normal saline was administered. The patient was pale but alert. There was crusted blood in her mouth and nostrils without active bleeding or petechiae. Her tongue was pierced with a ring, and sclerae were anicteric. Bleeding was noted from both nipples. There was no heart murmur or gallop, and jugular venous pressure was not elevated. Pulmonary exam revealed bibasilar crackles. Abdomen was soft, not tender, and without hepatosplenomegaly, and her umbilicus was pierced by a ring. Genitourinary exam revealed scant vaginal discharge and clotted blood in the vagina. Skin demonstrated no petechiae, ecchymoses, or stigmata of liver disease. Neurological and joint exams were normal.

It is hard to conceive of vaginal bleeding producing this profound a degree of hypotension. The patient may have additional occult sites of bleeding, or she may have a distributive cause of hypotension such as sepsis or adrenal hemorrhage with resultant adrenal insufficiency. Breast bleeding is unusual, even with profound thrombocytopenia, and I wonder about a concomitant factor deficiency. Furthermore, if thrombocytopenia was the sole reason for the bleeding, I would have expected petechiae. Diffuse vascular injury, such as from lupus or vasculitis, would be an unusual cause of profound bleeding unless there was also disseminated intravascular coagulation.

Laboratory studies revealed a white count of 2000/mm3, of which 42% were neutrophils, 40% bands, 8% lymphocytes, and 10% monocytes. Hematocrit was 17.6%, platelets 35,000/mm3. Sodium was 124 mmol/L, potassium 6 mmol/L, chloride 92 mmol/L, bicarbonate 10 mmol/L, blood urea nitrogen 122 mg/dL (43.5 mmol/L), and creatinine 3.4 mg/dL (300 mol/L). Blood glucose was 44 mg/dL (2.44 mmol/L). Total bilirubin was 3.0 mg/dL (51.3 mol/L; normal range, 0.1‐1.5), alkaline phosphatase 105 U/L (normal range, 39‐117), aspartate aminotransferase 849 U/L (normal range, 8‐31), alanine aminotransferase 261 U/L (normal range, 7‐31), international normalized unit (INR) 2.9, and partial thromboplastin time (PTT) 34.2 seconds.

The combination of profound hypotension, electrolyte abnormalities, hypoglycemia, and hypothermia makes adrenal insufficiency a consideration. I would perform a cortrosyn stimulation test and start glucocorticoid and perhaps mineralocorticoid replacement. In addition, there is renal failure and metabolic acidosis, with a calculated anion gap of 22. The anion gap may be from lactic acidosis secondary to hypotension and hypoperfusion. The abnormal transaminases and bilirubin could relate to infectious hepatitis or systemic infection. Although ischemia could explain these findings, it is rare for a 20‐year‐old to develop ischemic hepatopathy. Thrombocytopenia this moderate may augment the volume of blood loss, but spontaneous bleeding because of thrombocytopenia is unusual until the platelet count falls below 20,000/mm3. Furthermore, the elevated INR points to a mixed coagulopathy. Interpretation of the INR is complicated by the fact she has liver disease, and I am most concerned about acute disseminated intravascular coagulation (DIC) or impending fulminant hepatic failure. This is not the pattern seen with antiphospholipid antibody syndrome, in which the INR tends to be preserved and the PTT prolonged.

Urine dipstick testing demonstrated a specific gravity of 1.015, trace leukocyte esterase, 2+ protein, and 3+ blood, and microscopy revealed 2 white blood cells and 38 red blood cells per high‐power field, many bacteria, and no casts. Creatine kinase was 20,599 U/L, with a myocardial fraction of 1.4%. Lipase was normal, lactate was 7.3 mmol/L, and serum pregnancy test was negative.

Although there is proteinuria and hematuria, we do not have solid evidence of glomerulonephritis. Although the red cells could be a contaminant from her vaginal bleeding, I would examine her sediment carefully for dysmorphic red cells, recognizing that only a quarter of people with glomerulonephritis have red‐cell casts. A urine protein‐to‐creatinine ratio would be useful for estimating the degree of proteinuria. The elevated creatine kinase indicates rhabdomyolysis. In a previously healthy young woman without evidence of cardiogenic shock, it would be unusual for hypotension to result in rhabdomyolysis. Infection and metabolic derangements are possible etiologies of rhabdomyolysis. Alternatively, coagulopathy might have produced intramuscular bleeding. The constellation of thrombocytopenia, anemia, and renal failure raises my suspicion that there is a thrombotic microangiopathy, such as thrombotic thrombocytopenic purpura (TTP) or hemolytic uremic syndrome (HUS). I would inspect a peripheral‐blood smear for schistocytes and evidence of microangiopathy.

The chest radiograph demonstrated low lung volumes, patchy areas of consolidation, and pulmonary edema. Heart size was normal, and there were no pleural effusions. On the first hospital day the patient required mechanical ventilation because of respiratory failure. She received 5 units of packed red blood cells, 2 units of fresh frozen plasma, and 1 unit of platelets. Vasopressor infusion was started, and a vascular catheter was placed for hemodialysis. Blood, respiratory, and urine cultures were sent, and methylprednisolone, piperacillin/tazobactam, and vancomycin were administered. D‐dimer was greater than 10,000 ng/mL, fibrinogen was 178 mg/dL, and lactate dehydrogenase was 1671 U/L (27 kat/L). The peripheral‐blood smear demonstrated 1+ schistocytes and no spherocytes. There were fewer white blood cells with bands and myelocytes, but no blasts.

The presence of schistocytes and the elevated lactate dehydrogenase point to a microangiopathic hemolytic process. Causes of microangiopathic hemolytic anemia include TTP, HUS, DIC, paraneoplastic conditions, and endothelial damage from malignant hypertension or scleroderma renal crisis. The INR and PTT will usually be normal in TTP and HUS. The depressed fibrinogen and elevated D‐dimer suggest that in response to severe bleeding, she is also clotting. DIC, possibly from a severe infection, would explain these findings. Alternatively, the multisystem organ failure may represent progression of SLE.

Additional serology studies detected antinuclear antibodies at 1:320 with a speckled pattern. Rheumatoid factor was not present, but antidouble‐stranded DNA and antiSmith antibodies were elevated. C3 was 30 mg/dL (normal range, 90‐180), C4 was 24 mg/dL (normal range, 16‐47), and the erythrocyte sedimentation rate was 53 mm/h.

The results of the additional lab tests support a diagnosis of lupus and thus a lupus flare, but I agree that antibiotics should be empirically administered while searching for an underlying infection that might mimic lupus. Apart from infection, severe lupus may be complicated by widespread vasculitis or catastrophic antiphospholipid antibody syndrome, which would necessitate high‐dose immunosuppressive therapy and anticoagulation, respectively.

Tests for antiphospholipid antibodies including lupus anticoagulant and for anticardiolipin antibodies were negative. The patient continued to require vasopressors, hemodialysis, and mechanical ventilation. On the fourth hospital day she developed a morbilliform rash over her trunk, face, and extremities. Skin over her right buttock became indurated and tender. On the sixth day of hospitalization the skin on her face, extremities, and palms began to desquamate (Fig. 1).

Figure 1
Photographic images from hospital day 6: (A) desquamating, degloving hand rash, (B) desquamating, degloving hand rash extending onto the dorsum of the arm. [Color figure can be viewed in the online issue, which is available at www.interscience.wiley.com.]

Regarding the rash, it is hard to differentiate the chicken from the egg. The rash may be a reaction to medication, or it may be a clue to a multiorgan disease. I am considering severe skin reactions like Stevens‐Johnson as well as bacterial toxin‐mediated diseases such as toxic shock syndrome. The criteria for toxic shock syndrome with multisystem involvement are very similar to those for lupus. In this case, a desquamating rash occurring on the heel of a multiorgan illness definitely points to toxic shock syndrome. In staphylococcal toxic shock cases, blood cultures are frequently negative, and the origin may elude detection, but of the sources identified, most have been wounds and soft‐tissue infections.

On hospital day 4, blood cultures from admission grew oxacillin‐sensitive Staphylococcus aureus in 4 of the 4 bottles. Magnetic resonance imaging of the thigh demonstrated extensive necrosis of multiple muscles (Fig. 2). The patient underwent muscle debridement in the operating room, and Gram's stain of the debrided muscle revealed Gram‐positive cocci. Following surgery, she rapidly improved. She no longer required dialysis and was eventually discharged home after completing a prolonged course of intravenous anti‐Staphylococcal antibiotics at a rehabilitation facility. Follow‐up urine testing on 2 occasions revealed 1.6 and 1.4 g of protein in 24‐hour collections, but serum creatinine remained normal, and microscopy demonstrated no dysmorphic red cells or red‐cell casts. Performance of a kidney biopsy was deferred. Other than transient arthralgia and malar rash, her lupus has been quiescent, and her prednisone dose was tapered to 5 mg daily. Six months after discharge she returned to school.

Figure 2
T1‐weighted MRI (with fat saturation) of the thighs. There is extensive liquefactive necrosis involving multiple thigh muscles that is greater in the left thigh than the right thigh.

COMMENTARY

Using the American College of Rheumatology (ACR) definition, systemic lupus erythematosus (SLE) is diagnosed when at least 4 criteria are met with a sensitivity and specificity above 95%. These criteria were developed for study purposes to differentiate SLE from other rheumatic diseases. At disease onset a patient may not meet the ACR threshold, but delaying treatment may be harmful. Data conflict on the probability of such patients eventually being classified as having SLE, with estimates ranging from less than 10% to more than 60%.1, 2 With SLE prominent in the differential diagnosis of a critically ill patient, hospitalists must consider the 3 most common causes of death in lupus patients: lupus crisis, severe infection, and thrombosis.3

Most exacerbations of SLE occur in one system, most commonly the musculoskeletal system, and are mild. However, 10% of patients a year will require high‐dose corticosteroids or cytotoxic agents for severe flares that can occur in any system affected by lupus and in 15% of cases may involve multiple sites simultaneously.4, 5 Diagnosing lupus flares remains challenging. Although pulmonary hemorrhage and red blood cell casts may strongly implicate active lupus in the lungs or kidneys, specific clinical and laboratory markers of lupus crisis are lacking. Several global indices reliably measure current disease status but are cumbersome, cannot be relied on solely for treatment decisions and have not been well studied in hospitalized patients.68 Fever, once a dependable harbinger of active lupus,9 cannot reliably discriminate lupus flares from infection. In 2 studies, Rovin et al. found that infection accounted for fever in all but one SLE outpatient taking prednisone and that in hospitalized SLE patients, failure of fevers to resolve within 48 hours of administering 20‐40 mg of prednisone daily strongly suggested infection.10 The laboratory findings provided general support for there being an SLE flare or an infection, but, as the discussant pointed out, these cannot be relied on exclusively to discriminate between the two. Results that suggest infection in an SLE patient include leukocytosis, increased band forms or metamyelocytes, and possibly elevated C‐reactive protein. Findings favoring SLE flare include leukopenia, low C3 or C4 (particularly for nephritis or hematologic flares) and elevated anti‐double‐stranded DNA antibodies for nephritis.1113 Without a clear gold standard for definitively determining a lupus crisis, it is diagnosed when clinical manifestations fit a pattern seen in SLE (nephritis, cerebritis, serositis, vasculitis, pneumonitis), the results of serology studies support this conclusion, and other plausible diagnoses are excluded.

Infection and active disease account for most ICU admissions of lupus patients. SLE and infection intertwine in 3 ways. First, SLE patients are predisposed to infection, possibly because of a variety of identified genetic abnormalities of immune function.14 Although community‐acquired bacteria and viruses account for most infections, lupus patients are vulnerable to a wide array of atypical and opportunistic pathogens. Clinical factors that augment this intrinsic risk include severity of the underlying SLE, flares of the central nervous system or kidneys, and use of immunosuppressive agents.14 The latter deserves particular attention, as a recent study found more than 90% of SLE patients admitted to an ICU with severe infection were taking corticosteroids prior to hospitalization.15 Second, infection may trigger a lupus flare. Third, features of severe lupus flares and infection may overlap. Differentiating between the 2 may be difficult, and the stakes are high, as SLE patients admitted to ICUs have a risk of death that is substantially higher (47%) than that of those without SLE (29%) and much greater than the overall risk of death for those with SLE, for whom 10‐year survival exceeds 90%.15

In addition to lupus crisis and infection, the differential diagnosis of acute multisystem disease in a patient with SLE includes catastrophic antiphospholipid syndrome (APS) and thrombotic thrombocytopenic purpura, 2 thrombotic microangiopathies to which SLE patients are predisposed. Thrombocytopenia and hemolytic anemia with schistocytes should raise suspicion of these diagnoses. Additional findings for TTP include fevers, altered mental status, acute renal failure, and elevated serum lactate dehydrogenase; however, prothrombin time should not be prolonged. Lupus anticoagulant or anticardiolipin antibodies are found in up to 30% of lupus patients, of whom 50%‐70% develop APS within 20 years, characterized by thrombosis or spontaneous abortions in the presence of antiphospholipid antibodies.16 Catastrophic APS is a rare subset of APS involving thromboses of multiple organs simultaneously and has a mortality rate of 50%.

In the present patient, an elevated INR, bleeding, hypotension, and the absence of antiphospholipid antibodies argued against TTP and APS, leading the discussant to focus on SLE and sepsis. Arthralgia, cytopenia, and the results of serology studies suggested a lupus crisis, but hypothermia, hypotension, and DIC pointed to severe infection. Empiric treatment of both conditions with corticosteroids and broad‐spectrum antibiotics was indicated, and ultimately the patient's condition was found to meet criteria for toxic shock syndrome (TSS) and SLE. TSS has rarely been reported in SLE1718 and poses a particularly difficult diagnostic challenge because a severe lupus flare can meet the diagnostic criteria for TSS (Table 1), especially early on, before the characteristic desquamating rash appears. Acuity of the illness increased the ante in this challenging case. Afraid not to treat a potentially life‐threatening condition, empiric treatment of severe lupus and sepsis was initiated. Attention then shifted to fraying, or unraveling, the knot linking infection and lupus. Ultimately, diagnoses of both TSS and SLE were established.

Criteria for Toxic Shock Syndrome
  • As listed in the Morbidity and Mortality Weekly Report.19

1. Fever > 38.9C
2. Hypotension (SBP 90 mm Hg)
3. Diffuse erythroderma
4. Desquamation, particularly of palms and soles (occurring 1‐2 weeks after onset of illness)
5. Involvement of 3 or more systems:
GI (vomiting or diarrhea at onset)
Muscular (CK > twice the upper limit of normal or severe myalgia)
Mucus membranes (vaginal, oropharyngeal, or conjunctival hyperemia)
Renal (pyuria; BUN or creatinine > twice the upper limit of normal)
Hepatic (bilirubin or transaminases > twice the upper limit of normal)
Hematologic (platelets < 100,000/mm3)
Central nervous system (altered mental status without localizing deficits unexplained by hypotension or fever)
In addition, negative cultures of blood, throat, and cerebrospinal fluid are expected (except for blood cultures in S. aureus TSS, which may be positive).

Acknowledgements

The authors thank Michael Chan, MD, and Shelley Gordon, MD, for their input on this manuscript.

References
  1. Greer JM,Panush RS.Incomplete lupus erythematosus.Arch Intern Med.1989;149:24732476.
  2. Lom‐Orta H,Alarcon‐Segovia D,Diaz‐Jouanen E.Systemic lupus erythematosus. Differences between patients who do, and who do not, fulfill classification criteria at the time of diagnosis.J Rheumatol.1980;7:831837.
  3. Cervera R,Khamashta MA,Font J, et al.Morbidity and mortality in systemic lupus erythematosus during a 10‐year period: a comparison of early and late manifestations in a cohort of 1,000 patients.Medicine (Baltimore).2003;82:299308.
  4. Gordon C,Sutcliffe N,Skan J,Stoll T,Isenberg DA.Definition and treatment of lupus flares measured by the BILAG index.Rheumatology.2003;42:13721379.
  5. Ehrenstein MR,Conroy SE,Heath J,Latchman DS,Isenberg DA.The occurrence, nature and distributions of flares in a cohort of patients with systemic lupus erythematosus: a rheumatologic view.Br J Rheumatol.1995;34:257260.
  6. Ward MM,Marx AS,Barry NN.Comparison of the validity and sensitivity to change of 5 activity indices in systemic lupus erythematosus.J Rheumatol.2000;27:664670.
  7. Walz LeBlanc BA,Gladman DD,Urowitz, MB.Serologically active clinically quiescent systemic lupus erythematosus—predictors of clinical flares.J Rheumatol.1994;21:22392241.
  8. Esdaile JM,Abrahamowicz M,Joseph L,MacKenzie T,Li Y,Danoff D.Laboratory tests as predictors of disease exacerbations in systemic lupus erythematosus. Why some tests fail.Arthritis Rheum.1996;39:370378.
  9. Stahl NI,Klippel JH,Decker JL.Fever in systemic lupus erythematosus.Am J Med.1979;67:935940.
  10. Rovin BH,Tang Y,Sun J, et al.Clinical significance of fever in the systemic lupus erythematosus patient receiving steroid therapy.Kidney Int.2005;68:747759.
  11. Sidiropoulos PI,Kritikos HD,Boumpas DT.Lupus nephritis flares.Lupus.2005;14:4952.
  12. Ho A,Barr SG,Magder LS,Petri M.A decrease in complement is associated with increased renal and hematologic activity in patients with systemic lupus erythematosus.Arthritis Rheum.2001;44:23502357.
  13. Petri M,Genovese M,Engle E,Hochberg M.Definition, incidence, and clinical description of flare in systemic lupus erythematosus. A prospective cohort study.Arthritis Rheum.1991;34:937944.
  14. Zandman‐Goddard G,Shoenfeld Y.Infections and SLE.Autoimmunity.2005;38:473485.
  15. Hsu CL,Chen KY,Yeh PS, et al.Outcome and prognostic factors in critically ill patients with systemic lupus erythematosus: a retrospective study.Critical Care.2005;9:R177R183.
  16. Levine JS,Branch DW,Rauch J.The Antiphospholipid Syndrome.N Engl J Med.2002;346:752763.
  17. Chan RMT,Graham HR,Birmingham CL.Toxic shock syndrome in a patient with systemic lupus erythematosus.Can Med Assoc J.1983;129:12011202.
  18. Huseyin TS,Maynard JP,Leach RD.Toxic shock syndrome in a patient with breast cancer and systemic lupus erythematosus.Eur J Surg Oncol.2001;27:330331.
  19. Case definitions for infectious conditions under public health surveillance.MMWR Recomm Rep.1997;46(RR‐10):39.
References
  1. Greer JM,Panush RS.Incomplete lupus erythematosus.Arch Intern Med.1989;149:24732476.
  2. Lom‐Orta H,Alarcon‐Segovia D,Diaz‐Jouanen E.Systemic lupus erythematosus. Differences between patients who do, and who do not, fulfill classification criteria at the time of diagnosis.J Rheumatol.1980;7:831837.
  3. Cervera R,Khamashta MA,Font J, et al.Morbidity and mortality in systemic lupus erythematosus during a 10‐year period: a comparison of early and late manifestations in a cohort of 1,000 patients.Medicine (Baltimore).2003;82:299308.
  4. Gordon C,Sutcliffe N,Skan J,Stoll T,Isenberg DA.Definition and treatment of lupus flares measured by the BILAG index.Rheumatology.2003;42:13721379.
  5. Ehrenstein MR,Conroy SE,Heath J,Latchman DS,Isenberg DA.The occurrence, nature and distributions of flares in a cohort of patients with systemic lupus erythematosus: a rheumatologic view.Br J Rheumatol.1995;34:257260.
  6. Ward MM,Marx AS,Barry NN.Comparison of the validity and sensitivity to change of 5 activity indices in systemic lupus erythematosus.J Rheumatol.2000;27:664670.
  7. Walz LeBlanc BA,Gladman DD,Urowitz, MB.Serologically active clinically quiescent systemic lupus erythematosus—predictors of clinical flares.J Rheumatol.1994;21:22392241.
  8. Esdaile JM,Abrahamowicz M,Joseph L,MacKenzie T,Li Y,Danoff D.Laboratory tests as predictors of disease exacerbations in systemic lupus erythematosus. Why some tests fail.Arthritis Rheum.1996;39:370378.
  9. Stahl NI,Klippel JH,Decker JL.Fever in systemic lupus erythematosus.Am J Med.1979;67:935940.
  10. Rovin BH,Tang Y,Sun J, et al.Clinical significance of fever in the systemic lupus erythematosus patient receiving steroid therapy.Kidney Int.2005;68:747759.
  11. Sidiropoulos PI,Kritikos HD,Boumpas DT.Lupus nephritis flares.Lupus.2005;14:4952.
  12. Ho A,Barr SG,Magder LS,Petri M.A decrease in complement is associated with increased renal and hematologic activity in patients with systemic lupus erythematosus.Arthritis Rheum.2001;44:23502357.
  13. Petri M,Genovese M,Engle E,Hochberg M.Definition, incidence, and clinical description of flare in systemic lupus erythematosus. A prospective cohort study.Arthritis Rheum.1991;34:937944.
  14. Zandman‐Goddard G,Shoenfeld Y.Infections and SLE.Autoimmunity.2005;38:473485.
  15. Hsu CL,Chen KY,Yeh PS, et al.Outcome and prognostic factors in critically ill patients with systemic lupus erythematosus: a retrospective study.Critical Care.2005;9:R177R183.
  16. Levine JS,Branch DW,Rauch J.The Antiphospholipid Syndrome.N Engl J Med.2002;346:752763.
  17. Chan RMT,Graham HR,Birmingham CL.Toxic shock syndrome in a patient with systemic lupus erythematosus.Can Med Assoc J.1983;129:12011202.
  18. Huseyin TS,Maynard JP,Leach RD.Toxic shock syndrome in a patient with breast cancer and systemic lupus erythematosus.Eur J Surg Oncol.2001;27:330331.
  19. Case definitions for infectious conditions under public health surveillance.MMWR Recomm Rep.1997;46(RR‐10):39.
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
361-366
Page Number
361-366
Article Type
Display Headline
A frayed knot
Display Headline
A frayed knot
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
California Pacific Medical Center, 2351 Clay Street, Suite 380, San Francisco, CA 94115
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Handoffs

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
Rites of passage

It was the second week after finishing my internal medicine residency. What a daunting experience it was to be a newly appointed attending physician. My hospital rounds were painfully slow because I would consult the Tarsacon pharmacopoeia and Uptodate prior to writing any orders or making clinical decisions. During this keystone phase of my career I had the privilege of taking care of Ms. S. It has been almost 2 years since, and I still think of her and what I learned taking care of her.

Ms. S was a woman in her eighties with end‐stage chronic obstructive pulmonary disease (COPD). She was a frequent flyer, as evidenced by the multiple discharge summaries appended to her chart. Her hospital course was predictably punctuated by frequent inpatient exacerbations of COPD, and every time I told her that she'd be discharged the next day I had to eat my own words. After much effort and pharmaceutical gymnastics she finally seemed to be improving. She went nearly 3 days without a significant exacerbation of her condition. I believed that with my medical prowess, I would be mankind's next savior. As I told her yet again that she'd be discharged the next day, she thanked me and said she hoped not to be readmitted any time soon. Making small talk I learned that she had been a nurse at the very same hospital, where she had spent close to 40 years discharging her responsibilities. We didn't know smoking was bad back theneverybody did it, she said. I commiserated and assured her that she was well on her way to recovery.

The next day as I zealously sauntered into the hospital, I thought of the fantastic job I had done managing Ms. S's COPD. I mentally patted myself on the back; after all I was a smart guy. As I went into her room, I saw to my utter horror that she was in the midst of a severe COPD exacerbation. I swung into action, barked orders to start nebulizers, gave her a huge dose of steroids, and put her on a monitor. Through the clutter of nurses starting their IVs and the beeping of monitors, she said her time had come and she was ready to die. I gently chided her, assuring her this was just another episode, no different from her previous ones. She looked frail and tired, and her eyes appeared sad and forlorn. I departed from her room to call the resident in the ICU, where I thought surely she would be better served.

The unit unsurprisingly had no beds immediately available. She would be moved as soon as the unit had a bed; meanwhile, the pulmonary physician was on his way to see her. I dashed back to her room to check on her. To my dismay she was in respiratory distress, unable to talk and using all she had just to breathe. On the table next to the bed she had scribbled on a piece of scrap paper: Let me go please, it is OK. Knowing how exhausted she was, it must have taken superhuman effort to write this. She already had advance directives and was a DNR/DNI, but now she was precipitously declining in front of my eyes. Visibly trembling, I went to the nursing station and called her sister to apprise her of the waning of Ms. S's condition. I had never been faced with a scenario like this before. Taking time to compose myself, I wrote an order to put Ms. S on a morphine drip. All the while I couldn't shake off a sense of being ineffectual. Was modern medicine powerless to help people like her? I hoped I was doing the right thing. The pulmonary physician concurred with what I was doing, giving me the validation I was seeking.

Her sister arrived expeditiously, and I filled her in on what had happened. She nodded in understanding and stated her sister had always said when her time was up, she wanted to be let go. Her next question was the one I dreaded: How long do you think she has? I was evasive, reflecting my discomfiture at being totally unprepared in such situations. It is hard to tell, maybe 24 to 48 hours, but these things are hard to predict, I answered her. Writing orders for comfort measures, I couldn't help feeling unqualified to be a doctor. This wasn't something I thought I'd have to grapple with.

Soon all of Ms. S's relatives near and far came in to see her. They spent time at her bedside, but the morphine had taken effect. She was sleeping and looked comfortable but was unable to participate in conversation.

The next day as I arrived at the hospital, there was a cloud of dread in my mind. Ms. S probably had passed away some time during the night. At the nursing station, I was informed that the predictable hadn't happened. I went into her room to find it full of her loved ones. Her sister looked haggard but calm, and Ms. S was sleeping. I asked how things were, and Ms. S's sister's eyes lit up. She woke up at 1 a.m. and spoke to us for 2 hours. We were all able to tell her how much we loved her. She asked about all the children in the family and told us how much she loved them. Thereafter she went to sleep. She woke up at 6 a.m., looked around, and said, Why the hell am I still alive? She went to sleep soon and has been sleeping ever since. Laughter broke out in the room. I laughed with them. This was all a new experience. So Ms. S had closure before she died. Her family seemed content in this sad hour.

Ms. S passed away shortly after that. Her family thanked me for making her comfortable. But initially I felt I had done nothing much. Then the realization of my role as a doctor finally hit home. Sometimes it is apposite to hold a patient's hand and let the inevitable happen rather than fret on the shortcomings of medicine. It is all right not to overintellectualize every clinical event. After all it is all about treating people, not a constellation of bodily organs. Sometimes less is more and all that is needed. I always look back on this experience every time I feel smug. Since then I have incorporated discussion about goals of care into my repertoire. Patients with multiple admissions for incurable diseases need special attention. I hope my personal growth involves approaching such patients with the empathy and compassion they need. Having such discussions also helps to prevent the frenzied panicking that usually accompanies the inevitable decline of patients with terminal illness. The increasing emphasis of medical school curricula on end‐of‐life care issues reflects these sentiments. A growing geriatric cohort with multiple and often chronic medical diagnoses makes these skills indispensable.

My personal credo has been profoundly influenced by Sir Robert Hutchison's Physician's Prayer. I first read it in medical school but revisited it shortly after my experience with Ms S. To my mind, it is still relevant and serves to keep me on an even keel when making difficult decisions.

From inability to let well alone, from too much zeal for the new and contempt for what is old, from putting knowledge before wisdom, science before art and cleverness before common sense, from treating patients as cases and from making the cure of the disease more grievous than the endurance of the same, good Lord deliver us.

Sir Robert Hutchison (1871‐1960)

Print and Online Resources

  1. Oxford Textbook of Palliative Medicine.

  2. Center to Advance Palliative Care: www.capc.org.

  3. American Academy of Hospice and Palliative Medicine: www.abhpm.org.

  4. International Association for Hospice and Palliative Care: www.hospicecare.com.

Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
378-379
Sections
Article PDF
Article PDF

It was the second week after finishing my internal medicine residency. What a daunting experience it was to be a newly appointed attending physician. My hospital rounds were painfully slow because I would consult the Tarsacon pharmacopoeia and Uptodate prior to writing any orders or making clinical decisions. During this keystone phase of my career I had the privilege of taking care of Ms. S. It has been almost 2 years since, and I still think of her and what I learned taking care of her.

Ms. S was a woman in her eighties with end‐stage chronic obstructive pulmonary disease (COPD). She was a frequent flyer, as evidenced by the multiple discharge summaries appended to her chart. Her hospital course was predictably punctuated by frequent inpatient exacerbations of COPD, and every time I told her that she'd be discharged the next day I had to eat my own words. After much effort and pharmaceutical gymnastics she finally seemed to be improving. She went nearly 3 days without a significant exacerbation of her condition. I believed that with my medical prowess, I would be mankind's next savior. As I told her yet again that she'd be discharged the next day, she thanked me and said she hoped not to be readmitted any time soon. Making small talk I learned that she had been a nurse at the very same hospital, where she had spent close to 40 years discharging her responsibilities. We didn't know smoking was bad back theneverybody did it, she said. I commiserated and assured her that she was well on her way to recovery.

The next day as I zealously sauntered into the hospital, I thought of the fantastic job I had done managing Ms. S's COPD. I mentally patted myself on the back; after all I was a smart guy. As I went into her room, I saw to my utter horror that she was in the midst of a severe COPD exacerbation. I swung into action, barked orders to start nebulizers, gave her a huge dose of steroids, and put her on a monitor. Through the clutter of nurses starting their IVs and the beeping of monitors, she said her time had come and she was ready to die. I gently chided her, assuring her this was just another episode, no different from her previous ones. She looked frail and tired, and her eyes appeared sad and forlorn. I departed from her room to call the resident in the ICU, where I thought surely she would be better served.

The unit unsurprisingly had no beds immediately available. She would be moved as soon as the unit had a bed; meanwhile, the pulmonary physician was on his way to see her. I dashed back to her room to check on her. To my dismay she was in respiratory distress, unable to talk and using all she had just to breathe. On the table next to the bed she had scribbled on a piece of scrap paper: Let me go please, it is OK. Knowing how exhausted she was, it must have taken superhuman effort to write this. She already had advance directives and was a DNR/DNI, but now she was precipitously declining in front of my eyes. Visibly trembling, I went to the nursing station and called her sister to apprise her of the waning of Ms. S's condition. I had never been faced with a scenario like this before. Taking time to compose myself, I wrote an order to put Ms. S on a morphine drip. All the while I couldn't shake off a sense of being ineffectual. Was modern medicine powerless to help people like her? I hoped I was doing the right thing. The pulmonary physician concurred with what I was doing, giving me the validation I was seeking.

Her sister arrived expeditiously, and I filled her in on what had happened. She nodded in understanding and stated her sister had always said when her time was up, she wanted to be let go. Her next question was the one I dreaded: How long do you think she has? I was evasive, reflecting my discomfiture at being totally unprepared in such situations. It is hard to tell, maybe 24 to 48 hours, but these things are hard to predict, I answered her. Writing orders for comfort measures, I couldn't help feeling unqualified to be a doctor. This wasn't something I thought I'd have to grapple with.

Soon all of Ms. S's relatives near and far came in to see her. They spent time at her bedside, but the morphine had taken effect. She was sleeping and looked comfortable but was unable to participate in conversation.

The next day as I arrived at the hospital, there was a cloud of dread in my mind. Ms. S probably had passed away some time during the night. At the nursing station, I was informed that the predictable hadn't happened. I went into her room to find it full of her loved ones. Her sister looked haggard but calm, and Ms. S was sleeping. I asked how things were, and Ms. S's sister's eyes lit up. She woke up at 1 a.m. and spoke to us for 2 hours. We were all able to tell her how much we loved her. She asked about all the children in the family and told us how much she loved them. Thereafter she went to sleep. She woke up at 6 a.m., looked around, and said, Why the hell am I still alive? She went to sleep soon and has been sleeping ever since. Laughter broke out in the room. I laughed with them. This was all a new experience. So Ms. S had closure before she died. Her family seemed content in this sad hour.

Ms. S passed away shortly after that. Her family thanked me for making her comfortable. But initially I felt I had done nothing much. Then the realization of my role as a doctor finally hit home. Sometimes it is apposite to hold a patient's hand and let the inevitable happen rather than fret on the shortcomings of medicine. It is all right not to overintellectualize every clinical event. After all it is all about treating people, not a constellation of bodily organs. Sometimes less is more and all that is needed. I always look back on this experience every time I feel smug. Since then I have incorporated discussion about goals of care into my repertoire. Patients with multiple admissions for incurable diseases need special attention. I hope my personal growth involves approaching such patients with the empathy and compassion they need. Having such discussions also helps to prevent the frenzied panicking that usually accompanies the inevitable decline of patients with terminal illness. The increasing emphasis of medical school curricula on end‐of‐life care issues reflects these sentiments. A growing geriatric cohort with multiple and often chronic medical diagnoses makes these skills indispensable.

My personal credo has been profoundly influenced by Sir Robert Hutchison's Physician's Prayer. I first read it in medical school but revisited it shortly after my experience with Ms S. To my mind, it is still relevant and serves to keep me on an even keel when making difficult decisions.

From inability to let well alone, from too much zeal for the new and contempt for what is old, from putting knowledge before wisdom, science before art and cleverness before common sense, from treating patients as cases and from making the cure of the disease more grievous than the endurance of the same, good Lord deliver us.

Sir Robert Hutchison (1871‐1960)

Print and Online Resources

  1. Oxford Textbook of Palliative Medicine.

  2. Center to Advance Palliative Care: www.capc.org.

  3. American Academy of Hospice and Palliative Medicine: www.abhpm.org.

  4. International Association for Hospice and Palliative Care: www.hospicecare.com.

It was the second week after finishing my internal medicine residency. What a daunting experience it was to be a newly appointed attending physician. My hospital rounds were painfully slow because I would consult the Tarsacon pharmacopoeia and Uptodate prior to writing any orders or making clinical decisions. During this keystone phase of my career I had the privilege of taking care of Ms. S. It has been almost 2 years since, and I still think of her and what I learned taking care of her.

Ms. S was a woman in her eighties with end‐stage chronic obstructive pulmonary disease (COPD). She was a frequent flyer, as evidenced by the multiple discharge summaries appended to her chart. Her hospital course was predictably punctuated by frequent inpatient exacerbations of COPD, and every time I told her that she'd be discharged the next day I had to eat my own words. After much effort and pharmaceutical gymnastics she finally seemed to be improving. She went nearly 3 days without a significant exacerbation of her condition. I believed that with my medical prowess, I would be mankind's next savior. As I told her yet again that she'd be discharged the next day, she thanked me and said she hoped not to be readmitted any time soon. Making small talk I learned that she had been a nurse at the very same hospital, where she had spent close to 40 years discharging her responsibilities. We didn't know smoking was bad back theneverybody did it, she said. I commiserated and assured her that she was well on her way to recovery.

The next day as I zealously sauntered into the hospital, I thought of the fantastic job I had done managing Ms. S's COPD. I mentally patted myself on the back; after all I was a smart guy. As I went into her room, I saw to my utter horror that she was in the midst of a severe COPD exacerbation. I swung into action, barked orders to start nebulizers, gave her a huge dose of steroids, and put her on a monitor. Through the clutter of nurses starting their IVs and the beeping of monitors, she said her time had come and she was ready to die. I gently chided her, assuring her this was just another episode, no different from her previous ones. She looked frail and tired, and her eyes appeared sad and forlorn. I departed from her room to call the resident in the ICU, where I thought surely she would be better served.

The unit unsurprisingly had no beds immediately available. She would be moved as soon as the unit had a bed; meanwhile, the pulmonary physician was on his way to see her. I dashed back to her room to check on her. To my dismay she was in respiratory distress, unable to talk and using all she had just to breathe. On the table next to the bed she had scribbled on a piece of scrap paper: Let me go please, it is OK. Knowing how exhausted she was, it must have taken superhuman effort to write this. She already had advance directives and was a DNR/DNI, but now she was precipitously declining in front of my eyes. Visibly trembling, I went to the nursing station and called her sister to apprise her of the waning of Ms. S's condition. I had never been faced with a scenario like this before. Taking time to compose myself, I wrote an order to put Ms. S on a morphine drip. All the while I couldn't shake off a sense of being ineffectual. Was modern medicine powerless to help people like her? I hoped I was doing the right thing. The pulmonary physician concurred with what I was doing, giving me the validation I was seeking.

Her sister arrived expeditiously, and I filled her in on what had happened. She nodded in understanding and stated her sister had always said when her time was up, she wanted to be let go. Her next question was the one I dreaded: How long do you think she has? I was evasive, reflecting my discomfiture at being totally unprepared in such situations. It is hard to tell, maybe 24 to 48 hours, but these things are hard to predict, I answered her. Writing orders for comfort measures, I couldn't help feeling unqualified to be a doctor. This wasn't something I thought I'd have to grapple with.

Soon all of Ms. S's relatives near and far came in to see her. They spent time at her bedside, but the morphine had taken effect. She was sleeping and looked comfortable but was unable to participate in conversation.

The next day as I arrived at the hospital, there was a cloud of dread in my mind. Ms. S probably had passed away some time during the night. At the nursing station, I was informed that the predictable hadn't happened. I went into her room to find it full of her loved ones. Her sister looked haggard but calm, and Ms. S was sleeping. I asked how things were, and Ms. S's sister's eyes lit up. She woke up at 1 a.m. and spoke to us for 2 hours. We were all able to tell her how much we loved her. She asked about all the children in the family and told us how much she loved them. Thereafter she went to sleep. She woke up at 6 a.m., looked around, and said, Why the hell am I still alive? She went to sleep soon and has been sleeping ever since. Laughter broke out in the room. I laughed with them. This was all a new experience. So Ms. S had closure before she died. Her family seemed content in this sad hour.

Ms. S passed away shortly after that. Her family thanked me for making her comfortable. But initially I felt I had done nothing much. Then the realization of my role as a doctor finally hit home. Sometimes it is apposite to hold a patient's hand and let the inevitable happen rather than fret on the shortcomings of medicine. It is all right not to overintellectualize every clinical event. After all it is all about treating people, not a constellation of bodily organs. Sometimes less is more and all that is needed. I always look back on this experience every time I feel smug. Since then I have incorporated discussion about goals of care into my repertoire. Patients with multiple admissions for incurable diseases need special attention. I hope my personal growth involves approaching such patients with the empathy and compassion they need. Having such discussions also helps to prevent the frenzied panicking that usually accompanies the inevitable decline of patients with terminal illness. The increasing emphasis of medical school curricula on end‐of‐life care issues reflects these sentiments. A growing geriatric cohort with multiple and often chronic medical diagnoses makes these skills indispensable.

My personal credo has been profoundly influenced by Sir Robert Hutchison's Physician's Prayer. I first read it in medical school but revisited it shortly after my experience with Ms S. To my mind, it is still relevant and serves to keep me on an even keel when making difficult decisions.

From inability to let well alone, from too much zeal for the new and contempt for what is old, from putting knowledge before wisdom, science before art and cleverness before common sense, from treating patients as cases and from making the cure of the disease more grievous than the endurance of the same, good Lord deliver us.

Sir Robert Hutchison (1871‐1960)

Print and Online Resources

  1. Oxford Textbook of Palliative Medicine.

  2. Center to Advance Palliative Care: www.capc.org.

  3. American Academy of Hospice and Palliative Medicine: www.abhpm.org.

  4. International Association for Hospice and Palliative Care: www.hospicecare.com.

Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
378-379
Page Number
378-379
Article Type
Display Headline
Rites of passage
Display Headline
Rites of passage
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
64 Robbins St., Waterbury, CT 06721
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Editorial

Article Type
Changed
Mon, 01/02/2017 - 19:34
Display Headline
The language of quality improvement: Therapy classes

As we approach the 6th year since the Institute of Medicine's Crossing the Quality Chasm offered a new vision for the American health care system, we still have a marked mismatch between the demand for health care quality and the supply of know‐how to deliver it. What the field of quality improvement (QI) still needs is merely this: QI practitioners in every care setting, a working vocabulary, a predictive framework for the mechanisms of reliable care, and rational therapies rigorously studied.13 Fortunately, the field of QI has attracted enough empiricistsworking in the lab of the hospital and other care settingsto lurch forward. But few would argue that we still have far less insight into the delivery of quality care than into the delivery of myocardial blood flow.

For ischemic heart disease we have classes of therapies, each of which is grounded in basic and clinical science: antiplatelets, beta‐blockers, vasodilators, lipid‐lowering agents. For care delivery we have the makings of analogous therapy classes, derived and introduced rather recently in a large review, Closing the Quality Gap: A Critical Analysis of the Quality Improvement Literature.4, 5 To facilitate their review of the evidence, the authors, including 2 prominent hospitalists, developed a new taxonomy of QI strategies (see Table 1). Though their effect size, relative efficacy, and interactions are not yet clear, many of these strategies can be applied to the inpatient setting, perhaps no less rationally than a well‐constructed antianginal regimen.

Taxonomy of Quality Improvement Strategies
QI Strategies Examples
  • Source: adapted from Shojania KG, et al. Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Volume 1, Series Overview and Methodology, 2004. Available at: http://www.ahrq.gov/downloads/pub/evidence/pdf/qualgap1/qualgap1.pdf

Provider education Conferences and workshops
Educational outreach visits (eg, academic detailing)
Distributed educational materials
Provider reminder systems Reminders in charts for providers
Computer‐based reminders for providers
Computer‐based decision support
Facilitated relay of clinical data to providers Transmission of clinical data from data source to hospital physician by means other than medical record, eg, page, e‐mail, phone call to hospitalist about clinically significant findings in postdischarge period
Audit and feedback of performance to providers Feedback of performance to individual providers
Quality indicators and reports
National/state quality report cards
Publicly released performance data
Benchmarkingprovision of outcomes data from top performers for comparison with provider's own data
Patient education Classes
Parent and family education
Patient pamphlets
Intensive education strategies promoting self‐management of chronic conditions
Promotion of self‐management Materials and devices promoting self‐management, eg, diabetes educator, pharmacist‐facilitated teaching of discharge medications
Patient reminder systems Postcards or calls to patients
Organizational or team change Case management, disease management
Multidisciplinary teams
Change from paper to computer‐based records
Increased staffing
Skill mix changes
Continuous quality improvement Interventions using an iterative process for assessing quality problems, developing solutions, testing their impacts, and then reassessing the need for further action, eg, PlanDoStudyAct
Financial incentives, regulation, and policy Provider directed:
Financial incentives based on achievement of performance goals
Alternative reimbursement systems (eg, fee‐for‐service, capitated payments)
Licensure requirements
Health system directed:
Initiatives by accreditation bodies (eg, residency work hour limits)
Changes in reimbursement schemes (eg, capitation, prospective payment, salaried providers)

Where in the pathophysiology of a hospital do these QI therapies act? A plurality target the level of the provider: provider education, provider reminders, audit‐and‐feedback of provider performance, and facilitated relay of clinical data to providers. Remaining strategies target the patient (patient education, promotion of self‐management, and patient reminders), the immediate system within which care is delivered (organizational change), and the methodology of problem solving (continuous quality improvement). Only one strategy (financial incentives, regulation, and policy) fails to act directly at the level of the patient or provider, arguably the only level at which care actually can be improved.6

The value of the Quality Gap taxonomy is still largely untapped. If QI researchers and practitioners were to adopt its language as a standard, we could ramp up the power with which we communicate, interpret, and ultimately conduct improvement initiatives. In this issue of the Journal of Hospital Medicine, Cohn and colleagues profile a quality improvement initiative that achieved an impressive new level of performance. For an inpatient metric with a baseline institutional performance of 47%and an international benchmark of 39%the investigators executed a QI initiative that appears to have raised the rate of VTE prophylaxis to 85%.7 Despite a study design that weakens validity (beforeafter without controls) and a setting that diminishes applicability (medical patients in a single academic center), the authors have made a solid contribution to the QI literature simply by using the Quality Gap taxonomy. The authors specifically name and profile at least 3 distinct classes of QI strategies: provider education, a provider reminder element (ie, decision support), and an audit‐and‐feedback layer.

Even though provider education is unlikely to be sufficient as a lone QI strategya large review showed consistent but only modest benefitsit is often necessary.8 The provider education executed by Cohn and colleagues was frequent and regular. In the beginning of each month the chief resident oriented incoming house staff about venous thromboembolism (VTE) risk factors and the need for prophylaxis. They were given decision support pocket cards. Posters on display in nurse and physician work areas highlighted VTE risk factors. The provider education element also included discussions with the division chief about the topic. As robust as it was, however, the provider education was just a single component of the larger QI effort.

The second element, decision support, included VTE risk factor pocket cards with prophylaxis options listed. Introduced initially with the provider education, the pocket cards were handed out monthly by the chief resident. It is critical to recognize this decision support layer as a distinct core QI strategyand that it may even be fundamental to the success of the other strategies. Placed into the clinical workflow as a durable item, the decision support pocket card has the power to overcome provider uncertainty at moments of medical decision making. Generally speaking, a decision support layer, whether a pocket card, computer alert, or algorithm on a preprinted order form, can function as a shared baseline. Shared baselines or protocols reduce unnecessary variation in practice, a common source of poor quality care. Any mechanism that encourages groups of providers to deliver the same recommended care to groups of similarly at‐risk patients, while allowing customization of the protocol to meet the special needs of any individual patient, will have the net effect of raising overall quality of care.

This QI initiative may have achieved its greatest performance gainsas well as its greatest loss in terms of applicability to other settingsfrom its third facet, the audit‐and‐feedback layer. As a QI strategy audit‐and‐feedback has been defined as a summary of clinical performance for health care providers or institutions, performed for a specific period of time and reported either publicly or confidentially.1 It has demonstrated small to moderate benefits, with variations in effect most likely related to the format.9 As profiled in this study, it is hard to imagine a more powerful audit‐and‐feedback arrangement. The division chief of General Internal Medicine not only performed the audits, but also directly delivered the feedback to the house staff. In a deliberate, systematic, and successful way the investigators constructively used an existing authority gradient to leverage the Hawthorne effect, a change in worker behavior triggered by knowledge of being observed. Although it contributed to the impressive new VTE prophylaxis rates, this component did diminish generalizability and sustainability. Nonacademic centers may struggle to replicate these results, a point the authors dutifully point out. But even other academic centers might struggle in the absence of an authority figure with comparable influence and dedication to VTE prophylaxis. At the study hospital itself, similar rates of improvement would not be expected in patient populations outside the purview of the division chief.

Several alternatives to the before‐after study design could have produced richer information. Simultaneous data on VTE prophylaxis rates in a nonintervention population in the same or a similar hospital could have controlled for background or secular effects. An interrupted time series design may even have been feasible and could have provided more confidence in causality and more information on effect size. For example, what would be the effect on performance, if any, with removal of the decision support pocket card at 10 or 15 months? How much would performance rebound after its reintroduction? What could we have learned had the authors chosen instead to measure performance after sequentially introducing each component?

Using the language of the Quality Gap taxonomy, what conclusions can we draw from this improvement initiative? The introduction of a portable provider reminder (the decision support pocket card), when preceded by a program of provider education and followed by high‐intensity audit‐and‐feedback within an existing provider hierarchy, may have the power to raise VTE prophylaxis rates to 85% over an 18‐month period. With the large effect size somewhat mitigating the design flaws that weaken causality, we might risk an inference that these 3 classes of QI strategies can be reasonably successful in combination. But would we introduce them in our own medical centers? Using the clarity afforded by the taxonomy, we can identify several potential limitations, all attributable to the specifics of the audit‐and‐feedback arrangement: stringent preconditions of the practice setting, guaranteed inability to spread the initiative to other patient populations within the same medical center, limited scalability to include other QI projects, and reliance on the role of a single individual. Although clopidogrel 300 mg daily in the last week of every month is one way to pursue antiplatelet activity, other schedules or alternative agents may be preferable for the vast majority of patients.

The taxonomy can be used to compare, contrast, and more fully understand other QI studies. For example, among acutely ill medical inpatients not receiving VTE prophylaxis, Kucher and colleagues found that an electronic alert nearly doubled prophylaxis rates compared to those in a control group.10 Before trying to emulate their experience, a similarly equipped hospital would do well to recognize that the electronic alert was deployed as a composite of provider education, provider reminder, and facilitated relay of clinical information strategies, increasing prophylaxis rates for high risk patients from a baseline of 85% to 88%.

On the 21st‐century side of the quality chasm there is still something to be learned from QI research that falls short of recently proposed standards.3 This may be true as long as the key question remains: what are the mechanisms of reliable and sustainable performance improvement? We have not yet reached the day where a predictive framework, the clarity of our inquiry, the rigor of our study design, and the strength of our evidence churn out coherent answers. But we do have insights from a wealth of ongoing QI activity triggered by such forces as the Institute for Healthcare Improvement's 100,000 Lives Campaign and the advent of mandatory public reporting of hospital performance measures. By adding to this primordial mix the taxonomy offered by Closing the Quality Gap and its uptake into our vernacular by reports such as the one by Cohn in this issue of the Journal of Hospital Medicine, we are acquiring the language and experience to conduct intelligent and intelligible QI research.

References
  1. Van Bokhoven MA,Kok G,van der Weijden T.Designing a quality improvement intervention: a systematic approach.Qual Saf Health Care.2003;12;215220.
  2. Grimshaw J,Eccles M,Tetroe J.Implementing clinical guidelines: current evidence and future implications.J Contin Educ Health Prof.2004;24(Suppl 1):S31S37.
  3. Davidoff F,Batalden P.Toward stronger evidence on quality improvement. Draft publication guidelines: the beginning of a consensus project.Qual Saf Health Care.2005;14:319325.
  4. Shojania KG,McDonald KM,Wachter RM,Owens DK.Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Vol.1, Series Overview and Methodology. Technical Review 9 (Contract No. 290‐02‐0017 to the Stanford University–UCSF Evidence‐based Practices Center). AHRQ Publication No. 04‐0051‐1.Rockville, MD:Agency for Healthcare Research and Quality,2004.
  5. Shojania KG,Ranji SR,McDonald KM, et al.Effects of quality improvement strategies for type 2 diabetes on glycemic control: a meta‐regression analysis.JAMA.2006;296:427440.
  6. Nelson EC,Batalden PB,Huber TP, et al.Microsystems in health care: Part 1. Learning from high‐performing front‐line clinical units.Jt Comm J Qual Improv.2002;28:472493.
  7. Tapson VF,Decousus H,Piovella F, et al.A multinational observational cohort study in acutely ill medical patients of Pharmacological thromboembolic prophylaxis practices in prevention of venous thromboembolism: findings of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).Blood.2003;102(Suppl):321a.
  8. Grimshaw JM,Thomas RE,MacLennan G, et al.Effectiveness and efficiency of guideline dissemination and implementation strategies.Health Technol Assess.2004;6:184.
  9. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  10. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977
Article PDF
Issue
Journal of Hospital Medicine - 1(6)
Page Number
327-330
Sections
Article PDF
Article PDF

As we approach the 6th year since the Institute of Medicine's Crossing the Quality Chasm offered a new vision for the American health care system, we still have a marked mismatch between the demand for health care quality and the supply of know‐how to deliver it. What the field of quality improvement (QI) still needs is merely this: QI practitioners in every care setting, a working vocabulary, a predictive framework for the mechanisms of reliable care, and rational therapies rigorously studied.13 Fortunately, the field of QI has attracted enough empiricistsworking in the lab of the hospital and other care settingsto lurch forward. But few would argue that we still have far less insight into the delivery of quality care than into the delivery of myocardial blood flow.

For ischemic heart disease we have classes of therapies, each of which is grounded in basic and clinical science: antiplatelets, beta‐blockers, vasodilators, lipid‐lowering agents. For care delivery we have the makings of analogous therapy classes, derived and introduced rather recently in a large review, Closing the Quality Gap: A Critical Analysis of the Quality Improvement Literature.4, 5 To facilitate their review of the evidence, the authors, including 2 prominent hospitalists, developed a new taxonomy of QI strategies (see Table 1). Though their effect size, relative efficacy, and interactions are not yet clear, many of these strategies can be applied to the inpatient setting, perhaps no less rationally than a well‐constructed antianginal regimen.

Taxonomy of Quality Improvement Strategies
QI Strategies Examples
  • Source: adapted from Shojania KG, et al. Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Volume 1, Series Overview and Methodology, 2004. Available at: http://www.ahrq.gov/downloads/pub/evidence/pdf/qualgap1/qualgap1.pdf

Provider education Conferences and workshops
Educational outreach visits (eg, academic detailing)
Distributed educational materials
Provider reminder systems Reminders in charts for providers
Computer‐based reminders for providers
Computer‐based decision support
Facilitated relay of clinical data to providers Transmission of clinical data from data source to hospital physician by means other than medical record, eg, page, e‐mail, phone call to hospitalist about clinically significant findings in postdischarge period
Audit and feedback of performance to providers Feedback of performance to individual providers
Quality indicators and reports
National/state quality report cards
Publicly released performance data
Benchmarkingprovision of outcomes data from top performers for comparison with provider's own data
Patient education Classes
Parent and family education
Patient pamphlets
Intensive education strategies promoting self‐management of chronic conditions
Promotion of self‐management Materials and devices promoting self‐management, eg, diabetes educator, pharmacist‐facilitated teaching of discharge medications
Patient reminder systems Postcards or calls to patients
Organizational or team change Case management, disease management
Multidisciplinary teams
Change from paper to computer‐based records
Increased staffing
Skill mix changes
Continuous quality improvement Interventions using an iterative process for assessing quality problems, developing solutions, testing their impacts, and then reassessing the need for further action, eg, PlanDoStudyAct
Financial incentives, regulation, and policy Provider directed:
Financial incentives based on achievement of performance goals
Alternative reimbursement systems (eg, fee‐for‐service, capitated payments)
Licensure requirements
Health system directed:
Initiatives by accreditation bodies (eg, residency work hour limits)
Changes in reimbursement schemes (eg, capitation, prospective payment, salaried providers)

Where in the pathophysiology of a hospital do these QI therapies act? A plurality target the level of the provider: provider education, provider reminders, audit‐and‐feedback of provider performance, and facilitated relay of clinical data to providers. Remaining strategies target the patient (patient education, promotion of self‐management, and patient reminders), the immediate system within which care is delivered (organizational change), and the methodology of problem solving (continuous quality improvement). Only one strategy (financial incentives, regulation, and policy) fails to act directly at the level of the patient or provider, arguably the only level at which care actually can be improved.6

The value of the Quality Gap taxonomy is still largely untapped. If QI researchers and practitioners were to adopt its language as a standard, we could ramp up the power with which we communicate, interpret, and ultimately conduct improvement initiatives. In this issue of the Journal of Hospital Medicine, Cohn and colleagues profile a quality improvement initiative that achieved an impressive new level of performance. For an inpatient metric with a baseline institutional performance of 47%and an international benchmark of 39%the investigators executed a QI initiative that appears to have raised the rate of VTE prophylaxis to 85%.7 Despite a study design that weakens validity (beforeafter without controls) and a setting that diminishes applicability (medical patients in a single academic center), the authors have made a solid contribution to the QI literature simply by using the Quality Gap taxonomy. The authors specifically name and profile at least 3 distinct classes of QI strategies: provider education, a provider reminder element (ie, decision support), and an audit‐and‐feedback layer.

Even though provider education is unlikely to be sufficient as a lone QI strategya large review showed consistent but only modest benefitsit is often necessary.8 The provider education executed by Cohn and colleagues was frequent and regular. In the beginning of each month the chief resident oriented incoming house staff about venous thromboembolism (VTE) risk factors and the need for prophylaxis. They were given decision support pocket cards. Posters on display in nurse and physician work areas highlighted VTE risk factors. The provider education element also included discussions with the division chief about the topic. As robust as it was, however, the provider education was just a single component of the larger QI effort.

The second element, decision support, included VTE risk factor pocket cards with prophylaxis options listed. Introduced initially with the provider education, the pocket cards were handed out monthly by the chief resident. It is critical to recognize this decision support layer as a distinct core QI strategyand that it may even be fundamental to the success of the other strategies. Placed into the clinical workflow as a durable item, the decision support pocket card has the power to overcome provider uncertainty at moments of medical decision making. Generally speaking, a decision support layer, whether a pocket card, computer alert, or algorithm on a preprinted order form, can function as a shared baseline. Shared baselines or protocols reduce unnecessary variation in practice, a common source of poor quality care. Any mechanism that encourages groups of providers to deliver the same recommended care to groups of similarly at‐risk patients, while allowing customization of the protocol to meet the special needs of any individual patient, will have the net effect of raising overall quality of care.

This QI initiative may have achieved its greatest performance gainsas well as its greatest loss in terms of applicability to other settingsfrom its third facet, the audit‐and‐feedback layer. As a QI strategy audit‐and‐feedback has been defined as a summary of clinical performance for health care providers or institutions, performed for a specific period of time and reported either publicly or confidentially.1 It has demonstrated small to moderate benefits, with variations in effect most likely related to the format.9 As profiled in this study, it is hard to imagine a more powerful audit‐and‐feedback arrangement. The division chief of General Internal Medicine not only performed the audits, but also directly delivered the feedback to the house staff. In a deliberate, systematic, and successful way the investigators constructively used an existing authority gradient to leverage the Hawthorne effect, a change in worker behavior triggered by knowledge of being observed. Although it contributed to the impressive new VTE prophylaxis rates, this component did diminish generalizability and sustainability. Nonacademic centers may struggle to replicate these results, a point the authors dutifully point out. But even other academic centers might struggle in the absence of an authority figure with comparable influence and dedication to VTE prophylaxis. At the study hospital itself, similar rates of improvement would not be expected in patient populations outside the purview of the division chief.

Several alternatives to the before‐after study design could have produced richer information. Simultaneous data on VTE prophylaxis rates in a nonintervention population in the same or a similar hospital could have controlled for background or secular effects. An interrupted time series design may even have been feasible and could have provided more confidence in causality and more information on effect size. For example, what would be the effect on performance, if any, with removal of the decision support pocket card at 10 or 15 months? How much would performance rebound after its reintroduction? What could we have learned had the authors chosen instead to measure performance after sequentially introducing each component?

Using the language of the Quality Gap taxonomy, what conclusions can we draw from this improvement initiative? The introduction of a portable provider reminder (the decision support pocket card), when preceded by a program of provider education and followed by high‐intensity audit‐and‐feedback within an existing provider hierarchy, may have the power to raise VTE prophylaxis rates to 85% over an 18‐month period. With the large effect size somewhat mitigating the design flaws that weaken causality, we might risk an inference that these 3 classes of QI strategies can be reasonably successful in combination. But would we introduce them in our own medical centers? Using the clarity afforded by the taxonomy, we can identify several potential limitations, all attributable to the specifics of the audit‐and‐feedback arrangement: stringent preconditions of the practice setting, guaranteed inability to spread the initiative to other patient populations within the same medical center, limited scalability to include other QI projects, and reliance on the role of a single individual. Although clopidogrel 300 mg daily in the last week of every month is one way to pursue antiplatelet activity, other schedules or alternative agents may be preferable for the vast majority of patients.

The taxonomy can be used to compare, contrast, and more fully understand other QI studies. For example, among acutely ill medical inpatients not receiving VTE prophylaxis, Kucher and colleagues found that an electronic alert nearly doubled prophylaxis rates compared to those in a control group.10 Before trying to emulate their experience, a similarly equipped hospital would do well to recognize that the electronic alert was deployed as a composite of provider education, provider reminder, and facilitated relay of clinical information strategies, increasing prophylaxis rates for high risk patients from a baseline of 85% to 88%.

On the 21st‐century side of the quality chasm there is still something to be learned from QI research that falls short of recently proposed standards.3 This may be true as long as the key question remains: what are the mechanisms of reliable and sustainable performance improvement? We have not yet reached the day where a predictive framework, the clarity of our inquiry, the rigor of our study design, and the strength of our evidence churn out coherent answers. But we do have insights from a wealth of ongoing QI activity triggered by such forces as the Institute for Healthcare Improvement's 100,000 Lives Campaign and the advent of mandatory public reporting of hospital performance measures. By adding to this primordial mix the taxonomy offered by Closing the Quality Gap and its uptake into our vernacular by reports such as the one by Cohn in this issue of the Journal of Hospital Medicine, we are acquiring the language and experience to conduct intelligent and intelligible QI research.

As we approach the 6th year since the Institute of Medicine's Crossing the Quality Chasm offered a new vision for the American health care system, we still have a marked mismatch between the demand for health care quality and the supply of know‐how to deliver it. What the field of quality improvement (QI) still needs is merely this: QI practitioners in every care setting, a working vocabulary, a predictive framework for the mechanisms of reliable care, and rational therapies rigorously studied.13 Fortunately, the field of QI has attracted enough empiricistsworking in the lab of the hospital and other care settingsto lurch forward. But few would argue that we still have far less insight into the delivery of quality care than into the delivery of myocardial blood flow.

For ischemic heart disease we have classes of therapies, each of which is grounded in basic and clinical science: antiplatelets, beta‐blockers, vasodilators, lipid‐lowering agents. For care delivery we have the makings of analogous therapy classes, derived and introduced rather recently in a large review, Closing the Quality Gap: A Critical Analysis of the Quality Improvement Literature.4, 5 To facilitate their review of the evidence, the authors, including 2 prominent hospitalists, developed a new taxonomy of QI strategies (see Table 1). Though their effect size, relative efficacy, and interactions are not yet clear, many of these strategies can be applied to the inpatient setting, perhaps no less rationally than a well‐constructed antianginal regimen.

Taxonomy of Quality Improvement Strategies
QI Strategies Examples
  • Source: adapted from Shojania KG, et al. Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Volume 1, Series Overview and Methodology, 2004. Available at: http://www.ahrq.gov/downloads/pub/evidence/pdf/qualgap1/qualgap1.pdf

Provider education Conferences and workshops
Educational outreach visits (eg, academic detailing)
Distributed educational materials
Provider reminder systems Reminders in charts for providers
Computer‐based reminders for providers
Computer‐based decision support
Facilitated relay of clinical data to providers Transmission of clinical data from data source to hospital physician by means other than medical record, eg, page, e‐mail, phone call to hospitalist about clinically significant findings in postdischarge period
Audit and feedback of performance to providers Feedback of performance to individual providers
Quality indicators and reports
National/state quality report cards
Publicly released performance data
Benchmarkingprovision of outcomes data from top performers for comparison with provider's own data
Patient education Classes
Parent and family education
Patient pamphlets
Intensive education strategies promoting self‐management of chronic conditions
Promotion of self‐management Materials and devices promoting self‐management, eg, diabetes educator, pharmacist‐facilitated teaching of discharge medications
Patient reminder systems Postcards or calls to patients
Organizational or team change Case management, disease management
Multidisciplinary teams
Change from paper to computer‐based records
Increased staffing
Skill mix changes
Continuous quality improvement Interventions using an iterative process for assessing quality problems, developing solutions, testing their impacts, and then reassessing the need for further action, eg, PlanDoStudyAct
Financial incentives, regulation, and policy Provider directed:
Financial incentives based on achievement of performance goals
Alternative reimbursement systems (eg, fee‐for‐service, capitated payments)
Licensure requirements
Health system directed:
Initiatives by accreditation bodies (eg, residency work hour limits)
Changes in reimbursement schemes (eg, capitation, prospective payment, salaried providers)

Where in the pathophysiology of a hospital do these QI therapies act? A plurality target the level of the provider: provider education, provider reminders, audit‐and‐feedback of provider performance, and facilitated relay of clinical data to providers. Remaining strategies target the patient (patient education, promotion of self‐management, and patient reminders), the immediate system within which care is delivered (organizational change), and the methodology of problem solving (continuous quality improvement). Only one strategy (financial incentives, regulation, and policy) fails to act directly at the level of the patient or provider, arguably the only level at which care actually can be improved.6

The value of the Quality Gap taxonomy is still largely untapped. If QI researchers and practitioners were to adopt its language as a standard, we could ramp up the power with which we communicate, interpret, and ultimately conduct improvement initiatives. In this issue of the Journal of Hospital Medicine, Cohn and colleagues profile a quality improvement initiative that achieved an impressive new level of performance. For an inpatient metric with a baseline institutional performance of 47%and an international benchmark of 39%the investigators executed a QI initiative that appears to have raised the rate of VTE prophylaxis to 85%.7 Despite a study design that weakens validity (beforeafter without controls) and a setting that diminishes applicability (medical patients in a single academic center), the authors have made a solid contribution to the QI literature simply by using the Quality Gap taxonomy. The authors specifically name and profile at least 3 distinct classes of QI strategies: provider education, a provider reminder element (ie, decision support), and an audit‐and‐feedback layer.

Even though provider education is unlikely to be sufficient as a lone QI strategya large review showed consistent but only modest benefitsit is often necessary.8 The provider education executed by Cohn and colleagues was frequent and regular. In the beginning of each month the chief resident oriented incoming house staff about venous thromboembolism (VTE) risk factors and the need for prophylaxis. They were given decision support pocket cards. Posters on display in nurse and physician work areas highlighted VTE risk factors. The provider education element also included discussions with the division chief about the topic. As robust as it was, however, the provider education was just a single component of the larger QI effort.

The second element, decision support, included VTE risk factor pocket cards with prophylaxis options listed. Introduced initially with the provider education, the pocket cards were handed out monthly by the chief resident. It is critical to recognize this decision support layer as a distinct core QI strategyand that it may even be fundamental to the success of the other strategies. Placed into the clinical workflow as a durable item, the decision support pocket card has the power to overcome provider uncertainty at moments of medical decision making. Generally speaking, a decision support layer, whether a pocket card, computer alert, or algorithm on a preprinted order form, can function as a shared baseline. Shared baselines or protocols reduce unnecessary variation in practice, a common source of poor quality care. Any mechanism that encourages groups of providers to deliver the same recommended care to groups of similarly at‐risk patients, while allowing customization of the protocol to meet the special needs of any individual patient, will have the net effect of raising overall quality of care.

This QI initiative may have achieved its greatest performance gainsas well as its greatest loss in terms of applicability to other settingsfrom its third facet, the audit‐and‐feedback layer. As a QI strategy audit‐and‐feedback has been defined as a summary of clinical performance for health care providers or institutions, performed for a specific period of time and reported either publicly or confidentially.1 It has demonstrated small to moderate benefits, with variations in effect most likely related to the format.9 As profiled in this study, it is hard to imagine a more powerful audit‐and‐feedback arrangement. The division chief of General Internal Medicine not only performed the audits, but also directly delivered the feedback to the house staff. In a deliberate, systematic, and successful way the investigators constructively used an existing authority gradient to leverage the Hawthorne effect, a change in worker behavior triggered by knowledge of being observed. Although it contributed to the impressive new VTE prophylaxis rates, this component did diminish generalizability and sustainability. Nonacademic centers may struggle to replicate these results, a point the authors dutifully point out. But even other academic centers might struggle in the absence of an authority figure with comparable influence and dedication to VTE prophylaxis. At the study hospital itself, similar rates of improvement would not be expected in patient populations outside the purview of the division chief.

Several alternatives to the before‐after study design could have produced richer information. Simultaneous data on VTE prophylaxis rates in a nonintervention population in the same or a similar hospital could have controlled for background or secular effects. An interrupted time series design may even have been feasible and could have provided more confidence in causality and more information on effect size. For example, what would be the effect on performance, if any, with removal of the decision support pocket card at 10 or 15 months? How much would performance rebound after its reintroduction? What could we have learned had the authors chosen instead to measure performance after sequentially introducing each component?

Using the language of the Quality Gap taxonomy, what conclusions can we draw from this improvement initiative? The introduction of a portable provider reminder (the decision support pocket card), when preceded by a program of provider education and followed by high‐intensity audit‐and‐feedback within an existing provider hierarchy, may have the power to raise VTE prophylaxis rates to 85% over an 18‐month period. With the large effect size somewhat mitigating the design flaws that weaken causality, we might risk an inference that these 3 classes of QI strategies can be reasonably successful in combination. But would we introduce them in our own medical centers? Using the clarity afforded by the taxonomy, we can identify several potential limitations, all attributable to the specifics of the audit‐and‐feedback arrangement: stringent preconditions of the practice setting, guaranteed inability to spread the initiative to other patient populations within the same medical center, limited scalability to include other QI projects, and reliance on the role of a single individual. Although clopidogrel 300 mg daily in the last week of every month is one way to pursue antiplatelet activity, other schedules or alternative agents may be preferable for the vast majority of patients.

The taxonomy can be used to compare, contrast, and more fully understand other QI studies. For example, among acutely ill medical inpatients not receiving VTE prophylaxis, Kucher and colleagues found that an electronic alert nearly doubled prophylaxis rates compared to those in a control group.10 Before trying to emulate their experience, a similarly equipped hospital would do well to recognize that the electronic alert was deployed as a composite of provider education, provider reminder, and facilitated relay of clinical information strategies, increasing prophylaxis rates for high risk patients from a baseline of 85% to 88%.

On the 21st‐century side of the quality chasm there is still something to be learned from QI research that falls short of recently proposed standards.3 This may be true as long as the key question remains: what are the mechanisms of reliable and sustainable performance improvement? We have not yet reached the day where a predictive framework, the clarity of our inquiry, the rigor of our study design, and the strength of our evidence churn out coherent answers. But we do have insights from a wealth of ongoing QI activity triggered by such forces as the Institute for Healthcare Improvement's 100,000 Lives Campaign and the advent of mandatory public reporting of hospital performance measures. By adding to this primordial mix the taxonomy offered by Closing the Quality Gap and its uptake into our vernacular by reports such as the one by Cohn in this issue of the Journal of Hospital Medicine, we are acquiring the language and experience to conduct intelligent and intelligible QI research.

References
  1. Van Bokhoven MA,Kok G,van der Weijden T.Designing a quality improvement intervention: a systematic approach.Qual Saf Health Care.2003;12;215220.
  2. Grimshaw J,Eccles M,Tetroe J.Implementing clinical guidelines: current evidence and future implications.J Contin Educ Health Prof.2004;24(Suppl 1):S31S37.
  3. Davidoff F,Batalden P.Toward stronger evidence on quality improvement. Draft publication guidelines: the beginning of a consensus project.Qual Saf Health Care.2005;14:319325.
  4. Shojania KG,McDonald KM,Wachter RM,Owens DK.Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Vol.1, Series Overview and Methodology. Technical Review 9 (Contract No. 290‐02‐0017 to the Stanford University–UCSF Evidence‐based Practices Center). AHRQ Publication No. 04‐0051‐1.Rockville, MD:Agency for Healthcare Research and Quality,2004.
  5. Shojania KG,Ranji SR,McDonald KM, et al.Effects of quality improvement strategies for type 2 diabetes on glycemic control: a meta‐regression analysis.JAMA.2006;296:427440.
  6. Nelson EC,Batalden PB,Huber TP, et al.Microsystems in health care: Part 1. Learning from high‐performing front‐line clinical units.Jt Comm J Qual Improv.2002;28:472493.
  7. Tapson VF,Decousus H,Piovella F, et al.A multinational observational cohort study in acutely ill medical patients of Pharmacological thromboembolic prophylaxis practices in prevention of venous thromboembolism: findings of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).Blood.2003;102(Suppl):321a.
  8. Grimshaw JM,Thomas RE,MacLennan G, et al.Effectiveness and efficiency of guideline dissemination and implementation strategies.Health Technol Assess.2004;6:184.
  9. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  10. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977
References
  1. Van Bokhoven MA,Kok G,van der Weijden T.Designing a quality improvement intervention: a systematic approach.Qual Saf Health Care.2003;12;215220.
  2. Grimshaw J,Eccles M,Tetroe J.Implementing clinical guidelines: current evidence and future implications.J Contin Educ Health Prof.2004;24(Suppl 1):S31S37.
  3. Davidoff F,Batalden P.Toward stronger evidence on quality improvement. Draft publication guidelines: the beginning of a consensus project.Qual Saf Health Care.2005;14:319325.
  4. Shojania KG,McDonald KM,Wachter RM,Owens DK.Closing the Quality Gap: A Critical Analysis of Quality Improvement Strategies. Vol.1, Series Overview and Methodology. Technical Review 9 (Contract No. 290‐02‐0017 to the Stanford University–UCSF Evidence‐based Practices Center). AHRQ Publication No. 04‐0051‐1.Rockville, MD:Agency for Healthcare Research and Quality,2004.
  5. Shojania KG,Ranji SR,McDonald KM, et al.Effects of quality improvement strategies for type 2 diabetes on glycemic control: a meta‐regression analysis.JAMA.2006;296:427440.
  6. Nelson EC,Batalden PB,Huber TP, et al.Microsystems in health care: Part 1. Learning from high‐performing front‐line clinical units.Jt Comm J Qual Improv.2002;28:472493.
  7. Tapson VF,Decousus H,Piovella F, et al.A multinational observational cohort study in acutely ill medical patients of Pharmacological thromboembolic prophylaxis practices in prevention of venous thromboembolism: findings of the International Medical Prevention Registry on Venous Thromboembolism (IMPROVE).Blood.2003;102(Suppl):321a.
  8. Grimshaw JM,Thomas RE,MacLennan G, et al.Effectiveness and efficiency of guideline dissemination and implementation strategies.Health Technol Assess.2004;6:184.
  9. Shojania KG,Grimshaw JM.Evidence‐based quality improvement: the state of the science.Health Aff (Millwood).2005;24(1):138150.
  10. Kucher N,Koo S,Quiroz R, et al.Electronic alerts to prevent venous thromboembolism among hospitalized patients.N Engl J Med.2005;352:969977
Issue
Journal of Hospital Medicine - 1(6)
Issue
Journal of Hospital Medicine - 1(6)
Page Number
327-330
Page Number
327-330
Article Type
Display Headline
The language of quality improvement: Therapy classes
Display Headline
The language of quality improvement: Therapy classes
Sections
Article Source
Copyright © 2006 Society of Hospital Medicine
Disallow All Ads
Correspondence Location
1364 Clifton Rd., Box M7, Atlanta, GA, 30322
Content Gating
Gated (full article locked unless allowed per User)
Gating Strategy
First Peek Free
Article PDF Media

Newman's Handy Dandy Admit Note

Article Type
Changed
Fri, 09/14/2018 - 12:39
Display Headline
Newman's Handy Dandy Admit Note

(Circle the appropriate answers.)

HISTORY OF PRESENT ILLNESS

This (0-109)-year-old (Asian, Black, Caucasian, Aleutian, Venusian) (male, female, other) presents with a (1, 7, 100)-(second, minute, day, year, century) history of (pain, swelling, itching, enlargement) of the (arm, chest, scrotum, uvula, pineal gland). (She/He/It) rates it as (11, 12, 20) out of 10. It is aggravated by (breathing, thinking, hang gliding, vigorous dancing, ennui) and alleviated by (acetaminophen, chocolate, high-dose morphine).

PAST MEDICAL HISTORY

Diabetes, hypertension, pineal insufficiency, Kluver-Bucy syndrome, rectal prolapse, Chagas disease, visceral larval migrans, ichthyosis, all of the above

PAST SURGICAL HISTORY

  • Transplant of the (heart, kidney, pancreas, amygdala, pineal gland)
  • ORIF of (humerus, femur, rear axle)
  • Hemorrhoidectomy, cholecystectomy, pancreatectomy, cerumen removal, all of the above

Imaging: (CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ALLERGIES

(Penicillin, sulfa, every known drug in existence except Demerol)

CURRENT MEDICATION

  • Insulin, metformin, Gila monster venom
  • Alpha blocker, calcium blocker, beta blocker, blocker blocker
  • Amoxicillin, “gorillacillin,” maggot extract, “mickeymycin”
  • SSRI, MAOI, TRIAD, ECT, DOA
  • (Thyroid, adrenal, pineal) gland extract

FAMILY HISTORY

Adopted, old age, some kind of cancer

SOCIAL HISTORY

  • Alcohol: (teetotaler, tippler, boozer, lush, no alcohol—only beer)—multiply by 10
  • Smoking: (never; three packs a day; not tobacco; old stogies I have found, short but not too big around)
  • Drugs: (Is this confidential?, Freon, whatever I can get my hands on)
  • Employment: (meter maid, sewer maintenance worker, JCAHO auditor, forensic proctologist, hospitologist)

REVIEW OF SYMPTOMS

  • (Chest pain, more chest pain, even more chest pain), (rectal, urinary, salivary) incontinence, (ears itch with urination, nose runs with defecation, small bugs crawling out of my skin), (short of breath, short of patience)
  • Stool is (sticky, floating, malodorous, frequent, shaped like the Statue of Liberty)
  • Double vision, tunnel vision, television, hyperacusis, hearing loss, could you repeat that?, halitosis, dysgeusia, dysphonia, “datphonia”
  • Abdominal (pain, cramping, crunches)

PHYSICAL EXAM

  • BP (0, 90, 140, 230, 290)/(0, 3, 90, 160)
  • Pulse (absent, irregularly irregularly irregular, tachycardic, tacky dresser) rate (0, 3, 84, 112, 190, 280)
  • Temperature (32.2, 36.8, 25 minutes at 450—baste often)
  • Normocephalic/atraumatic, bullet-headed, pointy-headed, hatchet in skull
  • Eyes (PERRLA, anisocoria, bloodshot, pinpoint dude)
  • Fundus exam (never can see them, cotton wool spots, cotton candy)
  • Ears (present, “hyperceruminic,” absent)
  • Mouth (macroglossia, foot in mouth, black hairy tongue, halitotic, skin of the teeth, wooden teeth)
  • Neck (supple without adenopathy, thick, multiple hickies, red)
  • Lungs (clear to auscultation and percussion—OK, I never really percussed; Velcro rales; egophonic; wheezy)
  • Heart (systolic, 5/6, even a medical student can hear) murmur (no, pericardial, aye there’s the) rub
  • Abdomen (scaphoid, pendulous, six-pack); bowel sounds (absent—was that you?)
  • Umbilicus (surgically absent, Sister Mary Joseph nodule, high lint content)
  • Extremities (extreme, all six present, night-clubbing)

NEURO EXAM

  • Reflexes (cremaster positive, anal wink intact)
  • Mentation (alert and oriented x3, catatonic, dogatonic)
  • Psychiatric (appropriate, psychotic, truly weird, bipolar, tripolar)
  • Skin (present, hideous thing growing on the patient’s face)

LABORATORY FINDINGS

Results of (CBC, ionized calcium, “citrulated ceruloplasmin,” complement levels, insult levels, saliva electrophoresis, urinary zinc level, melatonin level, and protein Q) all markedly abnormal.

 

 

IMAGING

(CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ASSESSMENT AND PLAN

  1. “Hyperlabemia:” Likely iatrogenic etiology, or not. Correct with supplemental lab results.
  2. Pain: Source unclear but probably malingering. Treat with excessive narcotics, thereby causing problems 3 and 4 (see below).
  3. Bowel obstruction: Discontinue narcotics. Place (NG tube, rectal tube, boob tube, multiple consults).
  4. Altered mental status: Baseline worsened by narcotics. Give benzodiazepines, antipsychotics, antihistamine, more narcotics; then intubate.
  5. Discharge planning: The patient is a rock and will be on service forever.
  6. Abnormal imaging: Perform further scans.
  7. Code status: (Full code, no code, Morse code)
  8. Pineal: Gland abnormal—consult the pineal gland service TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

Issue
The Hospitalist - 2006(12)
Publications
Sections

(Circle the appropriate answers.)

HISTORY OF PRESENT ILLNESS

This (0-109)-year-old (Asian, Black, Caucasian, Aleutian, Venusian) (male, female, other) presents with a (1, 7, 100)-(second, minute, day, year, century) history of (pain, swelling, itching, enlargement) of the (arm, chest, scrotum, uvula, pineal gland). (She/He/It) rates it as (11, 12, 20) out of 10. It is aggravated by (breathing, thinking, hang gliding, vigorous dancing, ennui) and alleviated by (acetaminophen, chocolate, high-dose morphine).

PAST MEDICAL HISTORY

Diabetes, hypertension, pineal insufficiency, Kluver-Bucy syndrome, rectal prolapse, Chagas disease, visceral larval migrans, ichthyosis, all of the above

PAST SURGICAL HISTORY

  • Transplant of the (heart, kidney, pancreas, amygdala, pineal gland)
  • ORIF of (humerus, femur, rear axle)
  • Hemorrhoidectomy, cholecystectomy, pancreatectomy, cerumen removal, all of the above

Imaging: (CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ALLERGIES

(Penicillin, sulfa, every known drug in existence except Demerol)

CURRENT MEDICATION

  • Insulin, metformin, Gila monster venom
  • Alpha blocker, calcium blocker, beta blocker, blocker blocker
  • Amoxicillin, “gorillacillin,” maggot extract, “mickeymycin”
  • SSRI, MAOI, TRIAD, ECT, DOA
  • (Thyroid, adrenal, pineal) gland extract

FAMILY HISTORY

Adopted, old age, some kind of cancer

SOCIAL HISTORY

  • Alcohol: (teetotaler, tippler, boozer, lush, no alcohol—only beer)—multiply by 10
  • Smoking: (never; three packs a day; not tobacco; old stogies I have found, short but not too big around)
  • Drugs: (Is this confidential?, Freon, whatever I can get my hands on)
  • Employment: (meter maid, sewer maintenance worker, JCAHO auditor, forensic proctologist, hospitologist)

REVIEW OF SYMPTOMS

  • (Chest pain, more chest pain, even more chest pain), (rectal, urinary, salivary) incontinence, (ears itch with urination, nose runs with defecation, small bugs crawling out of my skin), (short of breath, short of patience)
  • Stool is (sticky, floating, malodorous, frequent, shaped like the Statue of Liberty)
  • Double vision, tunnel vision, television, hyperacusis, hearing loss, could you repeat that?, halitosis, dysgeusia, dysphonia, “datphonia”
  • Abdominal (pain, cramping, crunches)

PHYSICAL EXAM

  • BP (0, 90, 140, 230, 290)/(0, 3, 90, 160)
  • Pulse (absent, irregularly irregularly irregular, tachycardic, tacky dresser) rate (0, 3, 84, 112, 190, 280)
  • Temperature (32.2, 36.8, 25 minutes at 450—baste often)
  • Normocephalic/atraumatic, bullet-headed, pointy-headed, hatchet in skull
  • Eyes (PERRLA, anisocoria, bloodshot, pinpoint dude)
  • Fundus exam (never can see them, cotton wool spots, cotton candy)
  • Ears (present, “hyperceruminic,” absent)
  • Mouth (macroglossia, foot in mouth, black hairy tongue, halitotic, skin of the teeth, wooden teeth)
  • Neck (supple without adenopathy, thick, multiple hickies, red)
  • Lungs (clear to auscultation and percussion—OK, I never really percussed; Velcro rales; egophonic; wheezy)
  • Heart (systolic, 5/6, even a medical student can hear) murmur (no, pericardial, aye there’s the) rub
  • Abdomen (scaphoid, pendulous, six-pack); bowel sounds (absent—was that you?)
  • Umbilicus (surgically absent, Sister Mary Joseph nodule, high lint content)
  • Extremities (extreme, all six present, night-clubbing)

NEURO EXAM

  • Reflexes (cremaster positive, anal wink intact)
  • Mentation (alert and oriented x3, catatonic, dogatonic)
  • Psychiatric (appropriate, psychotic, truly weird, bipolar, tripolar)
  • Skin (present, hideous thing growing on the patient’s face)

LABORATORY FINDINGS

Results of (CBC, ionized calcium, “citrulated ceruloplasmin,” complement levels, insult levels, saliva electrophoresis, urinary zinc level, melatonin level, and protein Q) all markedly abnormal.

 

 

IMAGING

(CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ASSESSMENT AND PLAN

  1. “Hyperlabemia:” Likely iatrogenic etiology, or not. Correct with supplemental lab results.
  2. Pain: Source unclear but probably malingering. Treat with excessive narcotics, thereby causing problems 3 and 4 (see below).
  3. Bowel obstruction: Discontinue narcotics. Place (NG tube, rectal tube, boob tube, multiple consults).
  4. Altered mental status: Baseline worsened by narcotics. Give benzodiazepines, antipsychotics, antihistamine, more narcotics; then intubate.
  5. Discharge planning: The patient is a rock and will be on service forever.
  6. Abnormal imaging: Perform further scans.
  7. Code status: (Full code, no code, Morse code)
  8. Pineal: Gland abnormal—consult the pineal gland service TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

(Circle the appropriate answers.)

HISTORY OF PRESENT ILLNESS

This (0-109)-year-old (Asian, Black, Caucasian, Aleutian, Venusian) (male, female, other) presents with a (1, 7, 100)-(second, minute, day, year, century) history of (pain, swelling, itching, enlargement) of the (arm, chest, scrotum, uvula, pineal gland). (She/He/It) rates it as (11, 12, 20) out of 10. It is aggravated by (breathing, thinking, hang gliding, vigorous dancing, ennui) and alleviated by (acetaminophen, chocolate, high-dose morphine).

PAST MEDICAL HISTORY

Diabetes, hypertension, pineal insufficiency, Kluver-Bucy syndrome, rectal prolapse, Chagas disease, visceral larval migrans, ichthyosis, all of the above

PAST SURGICAL HISTORY

  • Transplant of the (heart, kidney, pancreas, amygdala, pineal gland)
  • ORIF of (humerus, femur, rear axle)
  • Hemorrhoidectomy, cholecystectomy, pancreatectomy, cerumen removal, all of the above

Imaging: (CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ALLERGIES

(Penicillin, sulfa, every known drug in existence except Demerol)

CURRENT MEDICATION

  • Insulin, metformin, Gila monster venom
  • Alpha blocker, calcium blocker, beta blocker, blocker blocker
  • Amoxicillin, “gorillacillin,” maggot extract, “mickeymycin”
  • SSRI, MAOI, TRIAD, ECT, DOA
  • (Thyroid, adrenal, pineal) gland extract

FAMILY HISTORY

Adopted, old age, some kind of cancer

SOCIAL HISTORY

  • Alcohol: (teetotaler, tippler, boozer, lush, no alcohol—only beer)—multiply by 10
  • Smoking: (never; three packs a day; not tobacco; old stogies I have found, short but not too big around)
  • Drugs: (Is this confidential?, Freon, whatever I can get my hands on)
  • Employment: (meter maid, sewer maintenance worker, JCAHO auditor, forensic proctologist, hospitologist)

REVIEW OF SYMPTOMS

  • (Chest pain, more chest pain, even more chest pain), (rectal, urinary, salivary) incontinence, (ears itch with urination, nose runs with defecation, small bugs crawling out of my skin), (short of breath, short of patience)
  • Stool is (sticky, floating, malodorous, frequent, shaped like the Statue of Liberty)
  • Double vision, tunnel vision, television, hyperacusis, hearing loss, could you repeat that?, halitosis, dysgeusia, dysphonia, “datphonia”
  • Abdominal (pain, cramping, crunches)

PHYSICAL EXAM

  • BP (0, 90, 140, 230, 290)/(0, 3, 90, 160)
  • Pulse (absent, irregularly irregularly irregular, tachycardic, tacky dresser) rate (0, 3, 84, 112, 190, 280)
  • Temperature (32.2, 36.8, 25 minutes at 450—baste often)
  • Normocephalic/atraumatic, bullet-headed, pointy-headed, hatchet in skull
  • Eyes (PERRLA, anisocoria, bloodshot, pinpoint dude)
  • Fundus exam (never can see them, cotton wool spots, cotton candy)
  • Ears (present, “hyperceruminic,” absent)
  • Mouth (macroglossia, foot in mouth, black hairy tongue, halitotic, skin of the teeth, wooden teeth)
  • Neck (supple without adenopathy, thick, multiple hickies, red)
  • Lungs (clear to auscultation and percussion—OK, I never really percussed; Velcro rales; egophonic; wheezy)
  • Heart (systolic, 5/6, even a medical student can hear) murmur (no, pericardial, aye there’s the) rub
  • Abdomen (scaphoid, pendulous, six-pack); bowel sounds (absent—was that you?)
  • Umbilicus (surgically absent, Sister Mary Joseph nodule, high lint content)
  • Extremities (extreme, all six present, night-clubbing)

NEURO EXAM

  • Reflexes (cremaster positive, anal wink intact)
  • Mentation (alert and oriented x3, catatonic, dogatonic)
  • Psychiatric (appropriate, psychotic, truly weird, bipolar, tripolar)
  • Skin (present, hideous thing growing on the patient’s face)

LABORATORY FINDINGS

Results of (CBC, ionized calcium, “citrulated ceruloplasmin,” complement levels, insult levels, saliva electrophoresis, urinary zinc level, melatonin level, and protein Q) all markedly abnormal.

 

 

IMAGING

(CAT scan, PET scan, DOG scan, plain film, complex film, KUB, IVP, XYZ, molybdenum scan, Afghaniscan)—all suggest need for further imaging.

ASSESSMENT AND PLAN

  1. “Hyperlabemia:” Likely iatrogenic etiology, or not. Correct with supplemental lab results.
  2. Pain: Source unclear but probably malingering. Treat with excessive narcotics, thereby causing problems 3 and 4 (see below).
  3. Bowel obstruction: Discontinue narcotics. Place (NG tube, rectal tube, boob tube, multiple consults).
  4. Altered mental status: Baseline worsened by narcotics. Give benzodiazepines, antipsychotics, antihistamine, more narcotics; then intubate.
  5. Discharge planning: The patient is a rock and will be on service forever.
  6. Abnormal imaging: Perform further scans.
  7. Code status: (Full code, no code, Morse code)
  8. Pineal: Gland abnormal—consult the pineal gland service TH

Jamie Newman, MD, FACP, is the physician editor of The Hospitalist, consultant, Hospital Internal Medicine, and assistant professor of internal medicine and medical history, Mayo Clinic College of Medicine at the Mayo Clinic College of Medicine, Rochester, Minn.

Issue
The Hospitalist - 2006(12)
Issue
The Hospitalist - 2006(12)
Publications
Publications
Article Type
Display Headline
Newman's Handy Dandy Admit Note
Display Headline
Newman's Handy Dandy Admit Note
Sections
Disallow All Ads
Content Gating
No Gating (article Unlocked/Free)